Endometriosis (EMS) is a difficult gynecological disease to cure. Frizzled-7 (FZD7) has been shown to be associated with the development of EMS, but its specific mechanism remains unclarified. This study aims to explore the role of FZD7 in EMS.

This study aims to explore the efficacy of neutrophil membrane nanovesicles (NMNVs) in the treatment of acute kidney injury caused by sepsis (S-AKI). Moreover, its effects on renal function indicators in plasma [creatinine (CREA), urea (UREA)], oxidative stress factor [malondialdehyde (MDA)], inflammatory factor [myeloperoxidase (MPO), histone H4 (H4), and macrophage inflammatory protein-2 (MIP-2)] are studied. Sixty SPF grade adult male Wistar rats in a healthy state under natural infection were randomly divided into blank, LSP, and experimental groups, with 20 rats in each group. After 7 days of adaptive feeding, a S-AKI model was established in the control group and the experimental group. The control group was treated with red blood cell membrane nanovesicles (RBC-NVs), the experimental group was treated with NMNVs, and the blank group was normal rats. The clinical treatment and changes in renal function indicators of the tested rats were observed and recorded. The total effective rate of treatment in the experimental group was higher than that in the controlling group (P < 0.05). Moreover, 1 h after the construction of the S-AKI model, the CREA, UREA, MDA, MPO, H4, MIP-2 in the controlling group and experimental group were higher than those in the blank group. At 7 and 14 h after constructing S-AKI model, the CREA, UREA, MDA, MPO, H4, and MIP-2 in the controlling and experimental groups decreased. However, the above indicators in the experimental group were lower than those in the controlling group (P < 0.05), and the comparison between this group and the blank group showed P > 0.05. In summary, the efficacy of NMNV in treating S-AKI is significant, as it can reduce CREA, UREA, MDA, MPO, as well as H4 and MIP-2, effectively controlling disease progression.

The nutritional status of fish is essential for its health, experimental studies, and aquaculture practices. The current study investigated the impact of food deprivation on biochemical parameters, histology of skin, gill, and kidney tissues, and ultrastructure of gills in Clarias batrachus. Fish were subjected to food deprivation for 2, 7, and 15 days resulting in (a) significant increase in plasma cortisol levels, (b) no significant changes in plasma osmolality and plasma glucose content, and (c) significant decrease in liver and muscle glycogen contents. A substantial damage was detected in skin, gill, and kidney tissues with histological alterations in a time-dependent manner. Skin tissue displayed melanomacrophage aggregation, excoriated epidermis and dermis. In gill tissue, epithelial lifting, edema, desquamation, deformed secondary lamellae, and lamellar hyperplasia were observed. Kidney tissue exhibited degenerated tubules, melanomacrophage aggregations, and shrunken renal tubule. Scanning electron microscopy revealed that food deprivation-induced marked presence of mucus, chloride cells, and pavement cells with well-defined microridges and microbridges following 2 days, opening of chloride cells was more prominent after 7 days, while more mucus secretion was observed after 15 days. After food deprivation, alterations in biochemical and histological parameters, and ultrastructural changes in target tissues reflect physiological and morphological disturbances in fish. The novelty of this study is that these parameters can be considered as biomarkers of feeding stress in fish and fish health and can provide important insights for better aquaculture practices.

Chronic obstructive pulmonary disease (COPD) stands as a major contributor to mortality worldwide, with cigarette smoke being a primary causative factor. Acacetin has been reported to possess lung protective effects. However, the precise role and mechanism of Acacetin in COPD remains elusive. In this study, human bronchial epithelial cell line HBE135-E6E7 was treated with Acacetin under cigarette smoke extract (CSE) conditions. Cellular viability was assessed using CCK-8 and LDH kits. Reactive oxygen species (ROS) generation was tested with DCFH-DA staining. JC-1 staining was employed to examine the mitochondrial membrane potential (MMP). Additionally, hydroxynonenal (4-HNE) level was tested using immunofluorescence staining and mitochondrial lipid peroxidation was evaluated using MitoPeDPP staining. MitoSOX staining was used to detect mitochondrial (mito)-ROS. Fe level was measured using FerroOrange staining and the expression of ferroptosis-related proteins was detected with western blot. Besides, the binding between Acacetin and NRF2 was analyzed by molecular docking. The sequent NRF2 overexpression or knockdown was used to explore the regulation of Acacetin on NRF2/SLC7A11/GPX4 signaling. Results indicated that CSE significantly reduced the viability, augmented ROS generation and decreased MMP in HBE135-E6E7 cells, which were blocked by Acacetin addition. Moreover, Acacetin inhibited lipid peroxidation and ferroptosis in CSE-treated HBE135-E6E7 cells. Specifically, Acacetin targeted NRF2 and activated the NRF2/SLC7A11/GPX4 signaling in CSE-induced HBE135-E6E7 cells. Furthermore, NRF2 deficiency or ML-385 treatment notably restored the influences of Acacetin on oxidative stress and ferroptosis in HBE135-E6E7 cells challenged with CSE. In conclusion, Acacetin alleviated CSE-induced injury in HBE135-E6E7 cells by activating The NRF2/SLC7A11/GPX4 signaling to inhibit ferroptosis.

Inflammatory bowel disease is a collection of intestinal disorders that cause inflammation in the digestive tract. Prolonged inflammation in the gastrointestinal tract is a major risk factor for colorectal cancer. The objective of this study was to fucus on gene expression levels of (KRT-14; associated with epithelial cell integrity) and enhancer of zeste homolog-1 (EZH-2; involved in cellular proliferation) in a IBD rat model in order to rule out impact of nutraceuticals (pumpkin seed oil; PSO) as a complementary approach to conventional treatments of IBD. In the current study, IBD was induced using dextran sodium sulfate (DSS). Following acclimatization, rats were separated into three groups: the negative control, the positive control, and the treatment group. The DSS (1 ml/kg bw) was given to the positive control and treatment groups. Negative control was given only a normal diet. Pumpkin seed oil (PSO) was given orally as a treatment (0.5 ml/kg bw). Blood and colon tissue were obtained on the 5, 10, 14 and 18 days. Physical parameters, hematology, biochemical assays, gene expression, and histopathology were carried out. After statistical analyses, macroscopic parameters showed significant differences. Biochemical analyses revealed a significant (P ≤ 0.05) decrease in serum potassium concentrations, total cholesterol, triglycerides, total proteins, total oxidants status, and C-reactive proteins in PSO treated group as compared with positive control. Gene expression levels of KRT-14 and EZH2 were significantly (P ≤ 0.05) upregulated in PSO treated group as compared to positive control group. Histopathology revealed that pumpkin seed oil preserved the structural integrity of colon.

Salidroside, a natural herb, exerts considerable anti-tumor effects in various human cancers. Evidence unveils that Salidroside mediates gene expression to affect cancer progression. Our work intended to uncover the molecular mechanism of Salidroside functional role in keloid. Expression analysis for JAG1 and miR-26a-5p in tissues and cells was performed using qRT-PCR or western blotting. For functional analysis, cell proliferation, apoptosis and migration were ascertained by CCK-8, flow cytometry and Transwell assay, respectively. The putative binding relationship between JAG1 and miR-26a-5p was further confirmed by dual-luciferase reporter assay. Salidroside exerted pharmacological properties in keloid and impaired keloid fibroblast (KF) viability. JAG1 was upregulated in keloid tissues, and its expression was repressed by Salidroside in KFs. Salidroside depleted KF proliferation and migration but stimulated apoptosis, and JAG1 knockdown largely strengthened the functional effects of Salidroside. MiR-26a-5p interacted with JAG1 3'UTR and expressed with an opposite pattern with JAG1 in keloid. Inhibition of miR-26a-5p largely abolished the effects of JAG1 knockdown in Salidroside-treated KFs, leading to the recovery of KF aggressive behaviors. Salidroside blocked KF aggressive progression by upregulating miR-26a-5p to inhibit JAG1, which provided evidence on the anti-tumor effects of Salidroside in human keloid.

O-linked N-acetylglucosamine transferase (OGT)-catalyzed O-linked N-acetylglucosamine glycosylation (O-GlcNAcylation) is closely associated with diabetes progression. This study aims to investigate the mechanism of OGT in regulating endothelial dysfunction in gestational diabetes mellitus (GDM). Expressions of OGT, O-linked N-acetylglucosamine (O-GlcNAc), enhancer of zeste homolog 2 (EZH2), and HEK27me3 in human umbilical vein endothelial cells (HUVECs) and GDM-derived HUVECs (GDM-HUVECs) were assessed by western blot. RT-qPCR and western blot assays were used to test the OGT overexpression and EZH2 silencing levels. CCK-8, EdU, wound healing, and transwell invasion assays were used to analyze the cell proliferative, migratory, and invasive abilities. Tube formation assay was performed to evaluate angiogenesis ability of cells. Western blot assay was performed to estimate vascular endothelial growth factor (VEGF) and p-VEGFR2 levels in cells. The binding of O-GlcNAc and EZH2 after OGT overexpression was measured by Co-IP assay. The results showed that OGT, O-GlcNAc, EZH2, and HEK27me3 expressions were declined in GDM-HUVECs. OGT overexpression induced the proliferation, migration, and invasion of GDM-HUVECs, and also elevated angiogenesis and the expressions of VEGF and p-VEGFR2 in cells. O-GlcNAc, EZH2, and HEK27me3 expressions were upregulated after OGT overexpression. OGT upregulation induced the binding between O-GlcNAc and EZH2. EZH2 silencing attenuated the promotion of OGT overexpression on the proliferative, invasive, migratory, and angiogenic capacities of GDM-HUVECs. To be concluded, OGT overexpression stabilized EZH2 expression by promoting O-GlcNAcylation modification of EZH2, and further enhanced proliferation, migration, and invasion as well as angiogenesis of GDM-HUVECs. While these effects were decayed after EZH2 absenting. Overall, the modulation of OGT on endothelial dysfunction in GDM provides a novel perspective for the clinical treatment of GDM.

Synephrine, a protoalkaloid found in Citrus aurantium (CA) peels, exerts lipolytic, anti-inflammatory, and vasoconstrictive effects; however, its antioxidant activity remains unclear. In this study, electron spin resonance spectroscopy revealed that synephrine scavenged both hydroxyl and superoxide anion radicals. Several external stimuli, such as HO, X-rays, and ultraviolet (UV) radiation, cause stress-induced premature senescence (SIPS). As oxidative stress induces SIPS, we hypothesized that synephrine, an antioxidant, would suppress HO-induced premature senescence in WI-38 cells. Synephrine significantly decreased the reactive oxygen species levels induced by HO, thereby reducing lipid peroxidation, and oxidative DNA damage and preventing SIPS. Additionally, synephrine inhibited mitochondrial dysfunction in HO-treated WI-38 cells. The expression levels of p53, p21, and p16, which are involved in the induction of cell cycle arrest in SIPS, were significantly lower in synephrine-treated cells than in untreated cells. Our results indicate that synephrine inhibits HO-induced oxidative stress and mitochondrial dysfunction, suppressing premature senescence by inhibiting activation of the p53-p21 and p16-pRB pathways.

Histone acetylation is the process by which histone acetyltransferases (HATs) add an acetyl group to the N-terminal lysine residues of histones, resulting in a more open chromatin structure. Histone acetylation tends to increase gene expression more than methylation does. In the central nervous system (CNS), histone acetylation is essential for controlling the expression of genes linked to cognition and learning. Histone deacetylases (HDACs), "writing" enzymes (HATs), and "reading" enzymes with bromodomains that identify and localize to acetylated lysine residues are responsible for maintaining histone acetylation. By giving animals HDAC inhibitors (HDACis), it is possible to intentionally control the ratios of "writer" and "eraser" activity, which will change the acetylation of histones. In addition to making the chromatin more accessible, these histone acetylation alterations re-allocate the targeting of "readers," including the transcriptional co-activators, cAMP response element-binding protein (CBP), and bromodomain-containing protein 4 (Brd4) in the CNS. Conclusive evidence has shown that HDACs slow down the progression of Alzheimer's disease (AD) by reducing the amount of histone acetylation, decreasing the activity of genes linked to memory, supporting cognitive decline and Amyloid beta (Aβ) protein accumulation, influencing aberrant tau phosphorylation, and promoting the emergence of neurofibrillary tangles (NFTs). In this review, we have covered the therapeutic targets and functions of HDACs that might be useful in treating AD.

Blood components play a crucial role in maintaining human health and accurately detecting them is essential for medical diagnostics. A cutting-edge sensor utilizing PCF revealed to precisely identify a wide range of blood components with WBCs (white blood cells), RBCs (red blood cells), HB (hemoglobin), platelets, and plasma. A numerical analysis was performed using COMSOL Multiphysics software to assess the capabilities of the sensor. The sensor design features a hexagonal hollow core-based PCF with a circled air hole operating wavelength from 1.0 μm to 3.0 μm. This innovative PCF sensor exhibits outstanding sensitivity, achieving relative sensitivity values of approximately 97.45% for WBCs, 99.13% for HB, 99.61% for RBCs, 93.44% for plasma, and an impressive 99.42% for platelets, all at a wavelength of 1 μm in its optimized design and this design ensures reliable and highly accurate measurements for various blood components. The corresponding effective areas are 3.32 × 10 m for WBCs, 2.91 × 10 m for HB, 2.72 × 10 m for RBCs, 3.74 × 10 m for plasma, and 2.79 × 10 m for platelets, respectively. Furthermore, The sensor demonstrates exceptional performance with remarkably low confinement loss values of 3.032 × 10 dB/m for WBCs, 2.947 × 10 dB/m for HB, 3.147 × 10 dB/m for RBCs, 3.112 × 10 dB/m for plasma, and 3.205 × 10 dB/m for platelets, respectively. Additionally, the effective material loss is 5.43 × 10 cm for WBCs, 2.19 × 10 cm for HB, 1.27 × 10 cm for RBCs, 1.32 × 10 cm for plasma, and 1.58 × 10 cm for platelets. Therefore, this biosensor's outstanding sensing capabilities and innovative design make it ideal for industrial and medical applications, ensuring reliability and ease of use. The PCF-based sensor has great potential to transform optical communication applications. Its prosperity model and high sensitivity build it a valued device with the promise of addressing critical challenges in the place of biology, medicine, and communication systems. The sensor features Teflon (tetrafluoroethylene) as its background material, with air holes optimized in a five-ring structure for maximum efficiency and it is the ideal fiber material, offering excellent relative sensitivity and low confinement loss (CL). More than that, 3D printing is the ideal method for fabricating hexagonal hollow-core photonic crystal fiber (PCF) structures, allowing for the effective production of the advanced biosensor design.

Cancer Stem Cells (CSCs) play an important role in the development, resistance, and recurrence of many malignancies. These subpopulations of tumor cells have the potential to self-renew, differentiate, and resist conventional therapy, highlighting their importance in cancer etiology. This review explores the regulatory mechanisms of CSCs in breast, cervical, and lung cancers, highlighting their plasticity, self-renewal, and differentiation capabilities. CD44+/CD24- cells are a known marker for breast CSCs. Markers like as CD133 and ALDH have been discovered in cervical cancer CSCs. Similarly, in lung cancer, CSCs identified by CD44, CD133, and ALDH are linked to aggressive tumor behavior and poor therapy results. The commonalities between these tumors highlight the general necessity of targeting CSCs in treatment efforts. However, the intricacies of CSC activity, such as their interaction with the tumor microenvironment and particular signaling pathways differ between cancer types, demanding specialized methods. Wnt/β-catenin, Notch, and Hedgehog pathways are one of the essential signaling pathways, targeting them, may show ameliorative effects on breast, lung and cervical carcinomas and their respective CSCs. Pre-clinical data suggests targeting specific signaling pathways can eliminate CSCs, but ongoing clinical trials are on utilizing signaling pathway inhibitors in patients. In recent studies it has been reported that CAR T based targeting of specific markers may be used as combination therapy. Ongoing research related to nanobiotechnology can also play a significant role in diagnosis and treatment purpose targeting CSCs, as nanomaterials can be used for precise targeting and identification of CSCs. Further research into the targeting of signaling pathways and its precursors could prove to be right step into directing therapies towards CSCs for cancer therapy.

This study aimed to observe the mechanism of hydrogen (H) in a lung transplantation model simulated by pulmonary microvascular endothelial cells (PMVECs), which were divided into 5 groups. The blank group was the normal PMVECs. During cold ischemia period, PMVECs in the control, O, or H groups were aerated with no gas, O, or 3% H, and 3% H after transfected with a small interfering RNA targeting Nrf2 in the H+si-Nrf2 group. Treatment with O and H decreased the oxidative stress injury, inflammation, cell apoptosis, and attenuated energy metabolism compared with the control group (P < 0.05). And the H group showed a better outcome with the increased protein expression of the Nrf2 and HO-1, which were conversed in the H+si-Nrf2 group. In conclusion, H attenuated inflammation, oxidative stress injury, cell apoptosis, and maintained the balance between energy supply and demand in a rat PMVECs lung transplantation model via Nrf2/HO-1.

Icariside II exerts protective effects against various diseases; however, its specific effects on osteoarthritis (OA) remain unclear. Therefore, in this study, we aimed to investigate the effects of icariside II in an in vitro model of OA and analyze its action mechanisms. We established an in vitro OA model by treating a human chondrocyte cell line (CHON-001) with interleukin (IL)-1β, followed by treatment with different concentrations of icariside II. Cell viability was measured using the methyl thiazolyl tetrazolium assay, and the level of lactate dehydrogenase (LDH) released from cells was determined using the appropriate kit. Tumor necrosis factor (TNF)-α, IL-6, and IL-8 levels were determined via enzyme-linked immunosorbent assay. Flow cytometry was used to assess apoptosis. Apoptosisrelated protein expression levels and TNFAIP3-interacting protein 2 (TNIP2)/nuclear factor (NF)-κB signaling pathway were analyzed via reverse transcription-quantitative polymerase chain reaction and western blotting. Furthermore, TNIP2-small interfering RNA (siRNA) was used to determine whether the TNIP2/NF-κB pathway influences the effects of icariside II on OA. Results indicated that Icariside II did not exert any significant toxic effects on CHON-001 cells. It inhibited IL-1β-induced apoptosis and increase in LDH levels and enhanced the inflammatory response. Additionally, icariside II reversed the IL-1β-induced decrease in TNIP2 levels and increase in NF-κB phosphorylation. TNIP2-siRNA revealed that the TNIP2/NF-κB signaling pathway influenced the alleviating effects of icariside II on OA. In conclusion, our results revealed that icariside II attenuated IL-1β-induced inflammatory injury in chondrocytes by increasing TNIP2 expression and inhibiting NF-κB pathway activation, highlighting its therapeutic potential for OA.

Total glucosides of paeony (TGP) have been investigated for their effects on cardiomyocyte hypertrophy induced by angiotensin II (Ang II). In this study, rat cardiomyocyte H9c2 cells were treated with various doses of TGP (0, 12.5, 25, 50, 100, 200, and 400 μmol/L), and cell viability was assessed using the MTT method to determine an optimal dose. To establish the cardiomyocyte hypertrophy model, Ang II (1 μmol/L) was used. The experimental groups included the control (Ctrl) group, the hypertrophy group (Ang II), the TGP treatment group (TGP+Ang II), and a combined treatment group (TGP+Ang II+LY), where LY294002, a PI3K/Akt inhibitor, was used. The surface area of H9c2 cells was analyzed using image analysis software, and apoptosis was assessed via flow cytometry. Western blotting was employed to evaluate markers related to cell proliferation, cardiac hypertrophy, apoptosis, and autophagy, as well as the phosphorylation of the PI3K/Akt pathway. The results revealed that Ang II inhibited cell viability and increased cell surface area, apoptosis, and autophagy, all of which were significantly reversed by TGP treatment. Moreover, the addition of LY294002 partially attenuated the effects of TGP, reducing cell viability and promoting hypertrophy, apoptosis, and autophagy. Additionally, Ang II reduced PI3K/Akt signaling activity, while TGP restored it. LY treatment reversed the effects of TGP and suppressed the PI3K/Akt pathway. In conclusion, TGP improves cardiomyocyte hypertrophy induced by Ang II by activating the PI3K/Akt signaling pathway.

In the contemporary era of drug discovery, herbal treatments have demonstrated an unparalleled ability to produce anticancer drugs. An important part of the therapy of cancer is the use of plants and their by-products via analogues, which alter the tumor microenvironment and several signaling pathways. The objective of the current investigation was to conclude the rate at which the herbal medications quercetin (QT) and sulforaphane (SFN) repressed the growth of breast carcinoma cells in MDA-MB-231 by preventing the ERK/MAPK signaling systems. The cells were assessed for several studies after being subjected to different concentrations (0-70 µM) of QT and SFN (QT + SFN) for duration of 24 h. We investigated the combination that QT + SFN generated cytotoxicity using the MTT assay. The DCFH-DA staining technique was utilized to assess ROS. The protein spectra of survival of cells, cell cycle progression, and apoptosis were evaluated employing flow cytometry and western blotting. The consequences illustrated that the relative cytotoxicity of QT and SFN was roughly 28.74 μM and 39.87 μM for MDA-MB-231 cells, respectively. Following the 24-h incubation period, MDA-MB-231 cells exhibit considerable cytotoxicity when QT and SFN are combined, with IC values of 19.48 μM. Moreover, MCF-7 and MDA-MB-231 cells treated with QT and SFN concurrently showed substantial production of ROS and increased apoptotic signals. Consequently, because QT + SFN inhibit the production of ERK/MAPK/JNK/p38-based control of proliferation and cell cycle-regulating proteins, it has been considered a chemotherapeutic medication. To determine the extent to which the co-treatment induces apoptosis, more in vivo study will be required before they can be used commercially.

Intervertebral disc degeneration (IDD) is the main pathological factor resulting in low back pain (LBP), the leading cause of disability globally. Inflammatory response and extracellular matrix (ECM) degradation are critical pathological features in the development of IDD. Gastrodin (GAS), a phenol compound isolated from Gastrodia elata Blume, plays an anti-inflammatory role in experimental models of multiple human diseases. Our study aimed to elucidate whether GAS alleviates TNF-α-induced inflammation in nucleus pulposus (NP) cells and IDD in vivo. The cytotoxicity of GAS was assessed by CCK-8 assay. Rat primary NP cells were stimulated with TNF-α to induce inflammatory response. The expression of proinflammatory cytokines, catabolic genes, and anabolic genes was detected by RT-qPCR, western blotting, and immunofluorescence staining. NF-κB and MAPK pathway activation was determined through western blotting and immunofluorescence staining. The IDD rat model was established by using percutaneous needle puncture. The therapeutic effects of GAS were confirmed by histology analysis. We found that TNF-α stimulation enhanced proinflammatory cytokine (COX2, iNOS, IL-6, and IL-1β) expression in NP cells, which was reversed by GAS treatment. GAS offset TNF-α-induced upregulation in catabolic gene (MMP3, MMP9, and MMP13) expression and downregulation in anabolic gene (Collagen II, SOX9, and Aggrecan) expression. The loss of ECM in TNF-α-treated NP cells was mitigated by GAS treatment. Mechanically, GAS abolished TNF-α-induced increase in p-IKKα, p-IKKβ, p-IκBα, p-p65, p-ERK, p-p38, and p-JNK protein levels in NP cells. In puncture-induced IDD rat models, GAS administration improved intervertebral disc (IVD) structure, increased Collagen II expression, and reduced the levels of proinflammatory factors in IVDs. Overall, GAS alleviates the inflammation and ECM degradation in NP cells via inhibiting NF-κB and MAPK pathway activation and alleviates IDD in vivo, which may be a novel treatment strategy for IDD.

Cholinergic deficiency and neuroinflammation are the two main factors of Alzheimer's disease. Recent studies have shown that water-soluble ginseng oligosaccharides (WGOS) derived from Panax ginseng roots can protect against scopolamine-induced impairments in learning and memory. However, the fundamental mechanisms remain unclear for the most part. The purpose of this study was to examine the effect of WGOS on cholinergic function and protein levels of proinflammatory cytokines in the hippocampus of mice. Mice were first pretreated with WGOS or saline, and then treated with scopolamine to establish an Alzheimer's disease model. The cognition memory of the mice was assessed through the behavioral test. The effect of WGOS on the cholinergic system was evaluated by measuring acetylcholine (ACh) neurotransmitter concentration and acetylcholinesterase (AChE) activity in the hippocampus. Using ELISA, the inflammatory cytokines IL-1β and TNF-α in the hippocampus were identified. This study found that WGOS treatment prevented the scopolamine-induced impairment of mice's recognition memory, as seen by their enhanced object recognition. In addition, WGOS prevented the scopolamine-induced decrease in ACh concentration and increase in AChE activity. Moreover, WGOS treatment inhibited scopolamine-induced upregulation of the inflammatory proteins IL-1β and TNF-α. These findings suggest that the amelioration of scopolamine-induced cognitive impairment in mice by WGOS was a consequence of the control of cholinergic function and inflammatory response in the hippocampus. Our findings suggest that WGOS should be investigated as a dietary supplement or medication for the treatment of learning and memory disorders in humans.

Sensorineural hearing loss (SNHL) is an increasingly prevalent sensory disorder, but the underlying mechanisms remain poorly understood. Adaptor related protein complex 2 subunit beta 1 (AP2B1) has been indicated to be detectable in mature cochleae. Nonetheless, it is unclear whether AP2B1 is implicated in the progression of SNHL. Male CBA/J mice were exposed to 2-20 kHz broadband noise at 96 or 101 dB SPL to induce temporary or permanent threshold shifts (TTS or PTS). Auditory brainstem responses were measured for hearing loss evaluation. Bioinformatics analysis was used to predict the upstream miRNAs of Ap2b1. RT-qPCR and western blotting were utilized to determine miR-145b and AP2B1 expression in mouse cochleae. Luciferase reporter assay was implemented to verify the interaction between Ap2b1 and miR-145b. Bioinformatics analysis identified miR-145b as an upstream miRNA of Ap2b1. AP2B1 expression was decreased and miR-145b expression was increased in mouse cochleae after PTS noise exposure. miR-145b targeted and negatively regulated Ap2b1 in PTS noise-exposed mice. Depletion of miR-145b alleviated auditory threshold shifts and outer hair cell loss in mice with exposure to PTS noise. In conclusion, inhibition of miR-145b ameliorates noise-induced SNHL in mice by upregulating AP2B1 expression.

Silymarin, a flavonoid complex isolated from Silybum marianum, possesses various biological properties, including antioxidant, anti-inflammatory, anti-glycation, and hepatoprotective effects. In the present study, we investigated the effects of silymarin on the SPC212 human mesothelioma cell line. MTT and neutral red assays were performed to examine the cytotoxic effects of silymarin. The apoptotic effect was investigated using AO/EB and DAPI staining, and morphological changes were observed using H&E and May-Grünwald staining. Additionally, immunocytochemistry was performed to detect Bax, Bcl2, and PCNA. Our results indicated that silymarin has a dose-dependent cytotoxic effect on SPC212 cells, with an IC value of approximately 187.5 µM. Silymarin induces apoptotic hallmarks such as apoptotic bodies, cell shrinkage, and nuclear condensation. In conclusion, silymarin demonstrated cytotoxic and apoptotic effects as well as morphological changes in SPC212 human mesothelioma cells. Further detailed studies are warranted to explore the potential of silymarin as an anti-cancer agent.

Putranjiva roxburghii is an important medicinal plant utilized for remedy of female reproductive ailments. Its seed extract is being used as a uterine health booster due to the presence of several pharmaceutically important phytochemicals. However, the presence of phytochemicals in its leaf is still unexplored. The present study was designed to explore phytochemical finger printing and assessment of anti-oxidant and anti-inflammatory activities of hydroalcoholic leaf extract of P. roxburghii (HALEPR). The qualitative, quantitative phytochemical of flavonoid, phenol and HRA-MS analysis of HALEPR carried out along with antioxidant and in vitro membrane stabilization and protein denaturation assay of anti-inflammatory activity were have been analyzed. Results of qualitative phytochemical screening of HALEPR denotes the existence of phenol, flavonoids, alkaloids, coumarins, steroids, saponins, tannins, anthroquinone and carbohydrates. The quantitative phytochemical of flavonoid and phenol was done which revealed the presents of total phenol and flavonoid. High resolution accurate-mass spectrometry (HRA-MS) study was also done for the identification of bioactive compounds from the HALEPR, which showed the presence of various phytochemicals such as luteolin 3'- (3″-acetylglucuronide), luteolin 4'-methyl ether 7-glucoside, quercetin-3β-D-glucoside, 8-hydroxyluteolin 4'-methyl ether 8-glucuronide, quercetin 3-xylosyl- (1- > 2) -rha mnosyl- (1- > 6) -glucoside, quercetin-3β-D-glucoside, myricetin 3- (3-6-diacetylglucosyl) - (1- > 4) - (2″,3″-diacetylrhamnoside), apigetrin, isorhamnetin, catechin 7,3'-Di-O-β-D glucopyranoside, luteolin 7-methylglucuronide, apigenin-8-C-α -l-arabinopyranoside, naringenin 7- O-β-D-glucoside 6″-acetate,ohobanin, shogaol, ginkgetin and amoritin. The HELPER is shown to have the presence of anti-oxidant and anti-inflammatory activities as demonstrated by DPPH (1, 1-diphenyl,2-picrylhydrazyl) and membrane lysis assays. Our findings reveal the presence of phytochemicals in HALEPR that have significant antioxidant and anti-inflammatory activity. The bioactivities were identified using chemical characterization like HRA/MS and biological assessments like anti-inflammatory and antioxidant assays. Future research may focus on isolating specific molecules, conducting in vivo tests, and creating HALEPR-based formulations for clinical application as anti-inflammatory drugs.