Rhubarb, the Rhei radix et rhizoma (Da huang) is a member of the Polygonaceae family, included in the 2020 edition of the Chinese Pharmacopoeia, and is mainly distributed in Gansu, Sichuan, Qinghai, northwestern Yunnan, and eastern Tibet. Rhei radix et rhizoma is one of the most commonly used traditional Chinese medicines, processed into drinkable tablets in different concoctions for clinical use. Phytochemical studies showed that more than 170 compounds were isolated and identified from Rhei radix et rhizoma, including anthraquinones/anthrones (major constituents), stilbenes, chromones, flavonoids, tannins, and other compounds, etc. Rhei radix et rhizoma is an herb with a long history of traditional use and many potential therapeutic benefits. It can play the role of diarrhea, clearing heat in response to different combinations and concoctions. It is mainly used for the treatment of constipation, gastrointestinal function impairment, and other diseases. In addition, Rhei radix et rhizoma has significant antitumor, anti-inflammatory, antibacterial, hepato-renal protective, neuroprotective, hypolipidemic, and immunomodulatory activities. Its active constituents have anti-tumor, anti-inflammatory, anti-inflammatory and hepato-kidney protective properties. Although it is primarily used for gastrointestinal disorders, it may also have wider applications in various inflammatory and liver disorders. Therefore, further studies are needed to explore its full potential and mechanism of action. This paper reviews the research progress of Rhei radix et rhizoma in terms of botany, traditional use, chemistry, pharmacology, and clinical studies. It aims to provide a scientific basis for in-depth research and development of Rhei radix et rhizome resources.

Osteoarthritis (OA) is a chronic degenerative articular disease that leads to physical disability and reduced quality of life. The key pathological events in OA are cartilage degradation and synovial inflammation. Conventional therapies often lead to adverse effects that some patients are unwilling to endure. Traditional Chinese Medicines (TCMs) have long been known for their efficacy in treating OA with minimal side effects. The wingless-type (Wnt) signaling pathway is believed to play a role in OA progression, but there is still a lack of comprehensive understanding on how TCM may treat OA via the Wnt signaling pathway. This study aims to fill this gap by reviewing relevant research on the association between the Wnt signaling pathway and cartilage degradation and synovial inflammation in OA. Meanwhile, we also summarized and categorized TCMs and their active components, such as alkaloids, polysaccharides, flavonoids, sesquiterpene lactones, etc., which have shown varying efficacy in treating OA through modulation of the Wnt/[Formula: see text]-catenin signaling pathway. This work underscores the pivotal role of the Wnt signaling pathway in OA pathogenesis and progression, suggesting that targeting this pathway holds promise as a prospective therapeutic strategy for OA management in the future. TCMs and their active components have the potential to alleviate OA by modulating the Wnt signaling cascade. Harnessing TCMs and their active components to regulate the Wnt signaling pathway presents an encouraging avenue for delivering substantial therapeutic benefits to individuals with OA.

A newly proposed form of programmed cell death, ferroptosis, is distinct in cellular morphology, biochemical characteristics, and genetic characteristics from apoptosis, autophagy, and necrosis. Its mechanisms primarily encompass iron overload, lipid peroxidation, and amino acid metabolisms. Extensive research confirms that ferroptosis is linked to the onset and progression of various diseases that pose a threat to the central nervous system (CNS), offering new directions and targets for the mechanistic study and pharmacotherapy of CNS diseases. Traditional Chinese Medicine (TCM), encompassing herbal medicines (extracts, compound formulations, injections, etc.), acupuncture, and moxibustion, boasts advantages over other treatments, such as multi-pathway and multi-target approaches and high safety. TCM has also demonstrated good efficacy in treating CNS diseases. Numerous studies indicate that TCM can modulate ferroptosis to treat CNS diseases, showing promising research prospects. This paper briefly outlines the pathways and mechanisms of ferroptosis and systematically summarizes the current status and progress of TCM in regulating various CNS diseases through the ferroptosis pathway, providing new insights and directions for future TCM treatments of CNS diseases.

Hyperuricemia is a crucial feature of metabolic syndrome, characterized by elevated uric acid that causes urate crystal deposits in joints, kidneys, and subcutaneous tissues, resulting in gout and hyperuricemic nephropathy. The primary causes of uric acid metabolism disorder include overproduction and reduced excretion. The majority of uric acid in human body is derived from the breakdown of purine nucleotides. Overproduction of uric acid can result from increased concentration or activity of xanthine oxidase, the key enzyme responsible for uric acid synthesis. Alterations in the activity of proteins responsible for uric acid reabsorption and excretion can also affect serum uric acid. Many bioactive compounds derived from natural plants have been shown to inhibit xanthine oxidase activity to reduce uric acid production, modulate the activity of transport proteins to promote uric acid excretion, or alleviate oxidative stress and inflammation through various signaling pathways. These properties have garnered significant attention from researchers. In this paper, we first introduce the pathophysiological mechanisms of hyperuricemia, then summarize bioactive compounds with urate-lowering effects, and discuss their potential applications in treating hyperuricemia and its complications.

Cisplatin-evoked profound gastrointestinal symptomatology is one of the most common side effects of chemotherapy drugs, causing further gastrointestinal cell and intestinal mucosal injury. Ginsenoside Rh4 (G-Rh4), an active component extracted from red ginseng, possesses beneficial anti-oxidative and anti-apoptosis effects. This study aimed to assess the effectiveness of pharmacological intervention with G-Rh4 mitigating intestinal toxicity evoked by cisplatin in a murine model and in IEC-6 cells . Following oral administration for 10 days, G-Rh4 (10[Formula: see text]mg/kg and 20[Formula: see text]mg/kg) significantly increased the indicators of diamine oxidase (DAO) affected by cisplatin (20[Formula: see text]mg/kg) in mice, and histopathological analysis further indicated that G-Rh4 could effectively improve intestinal tissue morphology, as well as the expression of peroxisome proliferator-activated receptor-gamma coactivator 1 [Formula: see text] (PGC-1[Formula: see text] pathway and autophagy-related proteins. Moreover, experiments demonstrated that G-Rh4 exerted a concentration-dependent increase in cell viability, while also inhibiting cytotoxicity and abnormal rise of reactive oxygen species (ROS). Notably, ROS also activate PGC-1[Formula: see text] protein and mediate the occurrence of mitochondrial autophagy and apoptosis pathways. The molecular docking approach was employed to dock G-Rh4 with PGC-1[Formula: see text] and AMPK, revealing a binding energy of [Formula: see text]7.3[Formula: see text]kcal/mol and [Formula: see text]8.1[Formula: see text]kcal/mol and indicating a tight interaction between the components and the target. G-Rh4 could reduce the expression of autophagy-related protein p62/p53, reduce the accumulation of autophagy products, and promote the flow of autophagy. In conclusion, G-Rh4 exerted protective effects against cisplatin-induced intestinal toxicity, at least partially through PGC-1[Formula: see text]-mediated autophagy and apoptosis.

Fucoxanthin, sourced from marine brown algae, diatoms, and microalgae, is known to possess strong anti-inflammatory activity. To explore its intrinsic mechanism, we investigated its effects on acute lung injury (ALI) with an experiment using lipopolysaccharide (LPS)-induced RAW264.7 inflammatory cells and an ALI animal model. Fucoxanthin was observed to suppress the inflammatory response by reducing the levels of inflammatory markers such as PTGS2, iNOS, and TNF-α. Network pharmacology analysis revealed that fucoxanthin could potentially inhibit ferroptosis through 10 targets, including PTGS2. This was further confirmed by the dose-dependent increase in lipid peroxidation and Fe[Formula: see text] levels caused by fucoxanthin, as well as the regulation of ferroptosis-associated proteins ACSL4, SLC7A11, GPX4, and FTH1. Furthermore, fucoxanthin was found to significantly reduce the inflammatory response and ferroptosis in a mouse model of LPS-induced ALI. Further research revealed that fucoxanthin could raise the levels of [Formula: see text]-Glu-Cys and carbamyl glycine, which are intermediate metabolites of glutathione synthesis, in RAW264.7 cells. This implies that fucoxanthin can inhibit ferroptosis by regulating the [Formula: see text]-glutamyl cycle. Our research demonstrated that fucoxanthin is capable of activating phosphorylated STAT3 and raising the expression of Nrf2 and HO-1, implying that fucoxanthin may be able to prevent LPS-induced ferroptosis in ALI through the Nrf2/STAT3 pathway.

Acupuncture is widely accepted as a therapeutic treatment by patients and healthcare providers globally. The safety record has been well established in acupuncture practice although some rare adverse events (AEs) were reported in the literature. While acupuncture-related AEs are generally defined as any undesirable event that occurs in patients during acupuncture treatment that may or may not be associated with the treatment, acupuncture-related adverse reactions (ARs) are defined as any undesirable or harmful reaction induced by trained practitioners practicing acupuncture treatment with standard doses. In this review, we clarify the relationship between AEs and ARs. Furthermore, we compile a list of acupuncture-related AEs reported in systematic reviews and meta-analysis articles. We find that serious acupuncture-related AEs are rare, with serious AEs occurring at a rate of approximately 0.04-0.08 per 10,000 treatments. The most likely serious AEs are pneumothorax, central and peripheral nerve injuries, heart injuries, abdominal organ injuries, infections, and needle breakage. Commonly reported minor AEs include bruising, hematoma, or bleeding at the needling site, as well as vasovagal reactions such as tiredness, dizziness, fainting, or residual pain at insertion points. The analysis identifies contributing factors for serious AEs being deep needle penetration, incorrect acupoint selection, and improper needle manipulation. It also addresses infections caused by contaminated needles, environmental factors, and inadequate skin disinfection. Moreover, other serious AEs, like needle breakage, are mostly due to aggressive manipulation and repeated reheating. Importantly, most acupuncture-related AEs are preventable. To avoid such AEs, acupuncturists in clinical practice should carefully select needling areas, be aware of cautions and contraindications of acupuncture, maintain safe acupuncture depth and hygiene, and strictly adhere to standard operating procedures.

Due to their complex pathological mechanisms, neurodegenerative diseases have brought great challenges to drug development and clinical treatment. Studies have shown that many traditional Chinese medicines have neuroprotective pharmacological activities such as anti-inflammatory and anti-oxidation properties and have certain effects on improving the symptoms of neurodegenerative diseases and delaying disease progression. Flavonoids are the main active components of many traditional Chinese medicines for the treatment of neurodegenerative diseases. These compounds have a wide range of biological activities, including anti-inflammatory, anti-oxidative stress, regulation of autophagy balance, inhibition of apoptosis, and promotion of neuronal regeneration. This paper focuses on the neuroprotective effects of six common flavonoids: quercetin, rutin, luteolin, kaempferol, baicalein, and puerarin. It then systematically reviews their characteristics, mechanisms, and key signaling pathways, summarizes the common characteristics and laws of their neuroprotective effects, and discusses the significance of strengthening the research on the neuroprotective effects of these compounds, aiming to provide reference for more research and drug development of these substances as neuroprotective drugs.

Artemisinin (ART) and its derivatives, collectively referred to as artemisinins (ARTs), have been approved for the treatment of malaria for decades. ARTs are converted into dihydroartemisinin (DHA), the only active form, which is reductive . In this review, we provide a brief overview of the neuroprotective potential of ARTs and the underlying mechanisms on several of the most common neurodegenerative diseases, particularly considering their potential application in those associated with cognitive and motor impairments including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). ARTs act as autophagy balancers to alleviate AD and PD. They inhibit neuroinflammatory responses by regulating phosphorylation of signal transduction proteins, such as AKT, PI3K, ERK, NF-[Formula: see text]B, p38 MAPK, I[Formula: see text]B[Formula: see text]. In addition, ARTs regulate GABAergic signaling in a dose-dependent manner. Although they competitively inhibit the binding of gephyrin to GABAergic receptors, low doses of ARTs enhance GABAergic signaling. ARTs can also inhibit ferroptosis, activate the Akt/Bcl-2, AMPK, or ERK/CREB pathways to reduce oxidative stress, and maintain mitochondrial homeostasis, protecting neurons from oxidative stress injury. More importantly, ARTs structurally combine with and suppress [Formula: see text]-Amyloid (A[Formula: see text]-induced neurotoxicity, reduce P-tau, and maintain O-GlcNAcylation/Phosphorylation balance, leading to relieved pathological changes in neurodegenerative diseases. Collectively, these natural properties endow ARTs with unique potential for application in neurodegenerative diseases.

Liver fibrosis is a common complication of chronic liver disease, significantly affecting patients' quality of life and potentially leading to cirrhosis and hepatocellular carcinoma. Despite advancements in modern medicine, the treatment of liver fibrosis remains limited and challenging. Thus, identifying new therapeutic strategies is of great clinical importance. Signaling pathways related to liver fibrosis play a crucial regulatory role in immune response and inflammation. Aberrant activation of specific pathways, such as the NF-[Formula: see text]B signaling pathway, results in the overexpression of genes associated with liver inflammation and fibrosis, thereby promoting the progression of liver fibrosis. Chinese medicine offers unique potential advantages as a therapeutic approach. Recent studies have increasingly demonstrated that certain Chinese medicines can effectively treat liver fibrosis by regulating relevant signaling pathways. The active ingredients in these medicines can inhibit hepatic inflammatory responses and fibrotic processes by interfering with these pathways, thus reducing the severity of liver fibrosis. This paper aims to investigate the mechanisms of Chinese medicine in treating liver fibrosis and its modulation of related signaling pathways. Additionally, it discusses the prospects of the clinical application of these treatments and provides valuable references for further research and clinical practice.

Recent studies have witnessed the incorporation of herbal medicine into the management of Disorders of Gut-Brain Interactions (DGBIs), reflecting a paradigm shift toward holistic healing modalities. However, there still exists a substantial gap in comprehending the utilization of Traditional Chinese Medicine (TCM) for Irritable Bowel Syndrome (IBS), particularly beyond the confines of China. This study endeavors to bridge this knowledge gap by meticulously identifying existing guidelines, critically reviewing TCM practices, and crafting contemporary treatment recommendations. We systematically searched several databases to retrieve related evidence in June 2023. Firstly, we employed the AGREE II tool to evaluate the recommended for use of TCM in the treatment of IBS, establishing a structured treatment selection hierarchy for different TCM patterns of IBS patients. Subsequently, we conducted an expert questionnaire to gain insights into the common treatment methods and medication choices practiced by clinical TCM doctors. Based on CM theory and experts' opinions, IBS with predominant Diarrheal (IBS-D) is divided into five Chinese medicine syndrome patterns, and IBS with predominant Constipation (IBS-C) is classified to four. A total of 22[Formula: see text]CM prescriptions were recommended for the management of IBS, 13 for IBS-D and 9 for IBS-C. The findings provide IBS patients with enhanced treatment choices while offering clinical physicians more specific treatment regimens. This research is the first to conduct a comprehensive study that combines guidelines with real clinical practices in the realm of TCM IBS treatment. This serves as a foundation for providing more personalized treatment options and improving the quality of life for patients.

Isoliquiritigen (ISL), a constituent of licorice, has been shown to possess antitumorigenic effects in diverse cancer types. In this study, we observed that ISL suppressed breast tumor development significantly more effectively in immunocompetent mice than in immunocompromised ones. In exploring the cause of such a discrepancy, we detected robust tumor infiltration of CD8[Formula: see text] T lymphocytes in mice treated with ISL, not seen in tumors derived from vehicle-treated mice. Moreover, we found a dramatic reduction in PD-L1 in both experimental breast tumors and cultured breast cancer cells upon ISL treatment. In further experiments, we showed that ISL selectively elevated miR-200c in breast cancer and confirmed that PD-L1 mRNA is the target of miR-200c in both murine and human breast cancer cells. ISL suppression of PD-L1 was functionally linked to miR-200c/ZEB1/2 because (1) ISL diminished ZEB1/2; (2) knockdown of ZEB1/2 led to the disappearance of PD-L1; and (3) miR-200c antagomiR disabled ISL to reduce PD-L1. We found evidence that ISL reduced the level of PD-L1 by simultaneously intercepting the ERK and Src signaling pathways. In agreement with clinical finding that PD-L1 antibodies enhance efficacy of taxane-based therapy, we showed that ISL improved the tumoricidal effects of paclitaxel in an orthopedic murine breast tumor model. This study demonstrates that ISL-led tumor suppression acts through the augmentation of host antitumor immunity.

Breast cancer (BC) is the most frequently diagnosed malignancy in female patients. There is a significant lack of therapeutic strategies for BC, particularly triple-negative breast cancer (TNBC). Honokiol (HNK), a lignin extracted from the genus plant, has demonstrated numerous pharmacological effects. Therefore, this study aims to investigate the antitumor effect of HNK on BC cells and employ high-throughput sequencing to elucidate its potential mechanism. We found that HNK significantly inhibited proliferation and induced apoptosis on BC cell lines in a dose-dependent manner. Moreover, HNK treatment suppressed migration and colony formation and initiated the intrinsic apoptotic pathway specifically in MDA-MB-231 cells. High-throughput sequencing and bioinformatics analysis revealed that miR-148a-5p expression was significantly up-regulated, whereas CYP1B1 expression was down-regulated following HNK treatment. Importantly, survival analysis based on TCGA database showed high miR-148a-5p expression was correlated with a better prognosis for BC patients. Inhibition of miR-148a-5p by inhibitor not only increased cell viability but also attenuated apoptosis induced by HNK. Finally, a strong synergistic effect between HNK and paclitaxel was observed in vitro. In conclusion, our study validated the antitumor efficacy of HNK against human BC cells and elucidated its underlying mechanism through high-throughput sequencing, thereby providing compelling evidence for further exploration of the potential clinical application of HNK towards the treatment of BC.

Diabetic kidney disease (DKD) has become the primary cause of end-stage renal disease (ESRD), causing an urgent need for preventive strategies for DKD. Astragaloside I (ASI), a bioactive saponin extracted from (Fisch.) Bunge has been demonstrated to possess a variety of biological activities. This study investigates the therapeutic potential of ASI in DKD and the underlying molecular mechanism using mice and high glucose (HG)-induced SV40-MES-13 cells . The results indicated that ASI significantly ameliorated renal dysfunction and mitigated the pathological alterations in the renal tissues of mice. Moreover, ASI was found to reduce the levels of renal fibrosis makers and suppress the activation of TGF-[Formula: see text]1/Smad2/3 pathway in both mice and HG-induced SV40-MES-13 cells. Furthermore, ASI downregulated HDAC3 expression, upregulated Klotho expression, and enhanced Klotho release. ASI is directly bound to HDAC3, and the beneficial effects of ASI on Klotho/TGF-[Formula: see text]1/Smad2/3-mediciated renal fibrosis in DKD were reversed by the HDAC3 agonist ITSA-1. In conclusion, ASI attenuates renal fibrosis in DKD, and may act through concurrently inhibiting HDAC3 and TGF-[Formula: see text]1, thereby regulating HDAC3-mediciated Klotho/TGF-[Formula: see text]1/Smad2/3 pathway.

This study explores the anti-inflammatory properties of lupeol, a notable phytosterol found in various medicinal plants, highlighting its potential as a candidate for new drug development. We examined the effects of lupeol on heme oxygenase (HO)-1, cyclooxygenase (COX)-2, and inducible nitric oxide synthase (iNOS) in lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs), as well as its impact on inflammatory markers in the lung tissues of LPS-challenged mice. Lupeol treatment enhanced HO-1 production, inhibited nuclear factor (NF)-κB activity, and reduced levels of COX-2/prostaglandin E2 (PGE2) and iNOS/nitric oxide (NO). In addition, lupeol decreased the phosphorylation of signal transducer and activator of transcription 1 (STAT-1) and promoted the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2), enhancing its binding to the anti-oxidant response element (ARE) and subsequently reducing interleukin (IL)-1β expression. , lupeol significantly lowered iNOS expression and tumor necrosis factor (TNF)-α levels in bronchoalveolar lavage fluid from LPS-treated mice. These findings suggest that lupeol exerts its anti-inflammatory effects by modulating key signaling pathways, positioning it as a promising candidate for the development of novel therapeutics targeting pathological inflammation.

Phytochemical flavonoids have been proven to be effective in treating various disorders, including cardiovascular diseases. Acacetin is a natural flavone with diverse pharmacological effects, uniquely including atrial-selective anti-atrial fibrillation (AF) via the inhibition of the atrial specific potassium channel currents [Formula: see text] (ultra-rapidly delayed rectifier potassium current), [Formula: see text] (acetylcholine-activated potassium current), [Formula: see text] (calcium-activated small conductance potassium current), and [Formula: see text] (transient outward potassium current). [Formula: see text] inhibition by acacetin, notably, suppresses experimental J-wave syndromes. In addition, acacetin provides extensive cardiovascular protection against ischemia/reperfusion injury, cardiomyopathies/heart failure, autoimmune myocarditis, pulmonary artery hypertension, vascular remodeling, and atherosclerosis by restoring the downregulated intracellular signaling pathway of Sirt1/AMPK/PGC-1[Formula: see text] followed by increasing Nrf2/HO-1/SOD thereby inhibiting oxidation, inflammation, and apoptosis. This review provides an integrated insight into the capabilities of acacetin as a drug candidate for treating cardiovascular diseases, especially atrial fibrillation and cardiomyopathies/heart failure.

Recent research has extensively explored the intricate mechanisms that underlie the effectiveness of acupuncture, highlighting the importance of stimulating acupoints, the role of acupuncture techniques in managing diseases, and the interaction between meridian pathways and molecular processes. Studies have underscored the crucial role of acupuncture in activating neurons, modulating the immune system, and influencing vascular activity, all of which contribute significantly to its therapeutic benefits across a wide range of symptoms and conditions. Utilization of imaging modalities enables the identification of changes in cerebral blood flow, brain function, and regional glucose metabolism following acupuncture sessions. The interstitial fluid circulation network within meridians adheres to specific laws that facilitate the transportation of materials. Acupuncture initiates the release of neurotransmitters, neuropeptides, and immune factors, impacting pain perception, inflammation, and physiological functions. It influences the complex neuro-endocrine-immune network by activating pathways involving the nervous system, the hypothalamic-pituitary-adrenal axis, and immune responses. Moreover, acupuncture induces molecular modifications such as phosphorylation, methylation, and histone modification, leading to key molecular changes that ultimately result in anti-inflammatory effects and the regulation of immune responses.

, a rare and protected genus predominantly distributed across the Northern Hemisphere's temperate regions, has garnered global attention due to its significant potential in medical research and pharmaceutical development, bolstered by advancements in cultivation techniques and medical technology. This review primarily focuses on the chemical constituents and pharmacological activities of , underscoring the progress and potential of these components in clinical applications. Recent studies have revealed that contains not only taxane active components but also flavonoids and polysaccharides with distinct activities. These compounds from exhibit potent antitumor, anti-inflammatory, immunomodulatory, antibacterial, and antidiabetic properties with evident mechanisms of action. Notably, the representative compound, paclitaxel, has demonstrated significant efficacy in treating various cancers, such as ovarian, breast, and lung cancer. This paper also reviews the basic situation of drug formulations, with extracts primarily administered orally and monomeric taxanes typically via injection, reflecting a mature development stage with ongoing research into oral formulations. Finally, this review summarizes the pharmacokinetic characteristics of crucial compounds in , including their absorption, distribution, metabolism, and excretion patterns in the human body. These pharmacokinetic profiles provide crucial guidance for evaluating the overall dosing regimen of and its components. The paper concludes with a forward-looking analysis of the potential applications of these compounds in disease treatment, envisioning their role in the future of medical and pharmaceutical advancements.

Salvianolic acid B (SalB), among the most abundant bioactive polyphenolic compounds found in Bge., exerts therapeutic and protective effects against various diseases. Although some summaries of the activities of SalB exist, there is lack of a scientometric and in-depth review regarding disease therapy. In this review, scientometrics was employed to analyze the number of articles, publication trends, countries, institutions, keywords, and highly cited papers pertaining to SalB research. The scientometric findings showed that SalB exerts excellent protective effects on the heart, lungs, liver, bones, and brain, along with significant therapeutic effects against atherosclerosis (AS), Alzheimer's disease (AD), liver fibrosis, diabetes, heart/brain ischemia, and osteoporosis, by regulating signaling pathways and acting on specific molecular targets. Moreover, this review delves into in-depth insights and perspectives, such as the utilization of SalB in combination with other drugs, the validation of molecular mechanisms and targets, and the research and development of novel drug carriers and dosage forms. In conclusion, this review aimed to offer a comprehensive scientometric analysis and in-depth appraisal of SalB research, encompassing both present achievements and future prospects, thereby providing a valuable resource for the clinical application and therapeutic exploitation of SalB.

Osthole, a coumarin compound mainly derived from (L.), has attracted much interest from the scientific community owing to its multiple therapeutic properties. However, its pharmacological mechanism, pharmacokinetics, and toxicological effects are far from clear. Furthermore, the potential drug delivery platforms of osthole remain to be comprehensively delineated. The present review aimed to systematically summarize the most up-to-date information related to pharmacology, pharmacokinetics, and safety issues related to osthole, and discuss the investigations of novel drug delivery platforms. The information herein discussed was retrieved from authoritative databases, including PubMed, Web of Science, Google Scholar, Chinese National Knowledge Infrastructure (CNKI) and so on, reviewing information published up until February of 2024. New evidence shows that osthole induces a sequence of therapeutic actions and has a moderate absorption rate and rapid metabolic characteristics. In addition, this phytoconstituent possesses potential hepatotoxicity, and caution should be exercised against the risk of the drug combination. Furthermore, given its needy solubility in aqueous medium and non-organizational targeting, novel drug delivery methods have been designed to overcome these shortcomings. Given the properties of osthole, its therapeutic benefits ought to be elucidated in a greater array of comprehensive research studies, and the molecular mechanisms underlying these benefits should be explored.