bicyclol and Liver-Diseases

bicyclol has been researched along with Liver-Diseases* in 3 studies

Reviews

1 review(s) available for bicyclol and Liver-Diseases

ArticleYear
Therapeutic potential of bicyclol in liver diseases: Lessons from a synthetic drug based on herbal derivative in traditional Chinese medicine.
    International immunopharmacology, 2021, Volume: 91

    Bicyclol, an innovative chemical drug with proprietary intellectual property rights in China, is based on derivative of traditional Chinese medicine (TCM) Schisandra chinensis (Wuweizi) of North. Mounting data has proved that bicyclol has therapeutic potential in various pathological conditions in liver. In this narrative review, we provide the first summary of pharmacological activities, pharmacokinetic characteristics and toxicity of bicyclol, and discuss future research perspectives. Our results imply that bicyclol has a wide spectrum of pharmacological properties, including anti-viral, anti-inflammatory, immuno-regulatory, anti-oxidative, antisteatotic, anti-fibrotic, antitumor, cell death regulatory effects and modulation of heat shock proteins. Pharmacokinetic studies have indicated that bicyclol is the main substrate of CYP3A/2E1. Additionally, no obvious drug interactions have been found when bicyclol is administered simultaneously with other prescriptions. Furthermore, the results of chronic toxicity have strongly addressed that bicyclol has no noticeable toxic effects on all biochemical indices and pathological examinations of the main organs. In view of good pharmacological actions and safety, bicyclol is anticipated to be a potential candidate for various liver diseases, including acute liver injury, fulminant hepatitis, non-alcoholic fatty liver disease, fibrosis and hepatocellular carcinoma. Further studies are therefore required to delineate its molecular mechanisms and targets to confer this well-designed drug a far greater potency. We hope that bicyclol-based therapeutics for liver diseases might be broadly used in clinical practice worldwide.

    Topics: Animals; Biphenyl Compounds; Drugs, Chinese Herbal; Humans; Liver; Liver Diseases; Medicine, Chinese Traditional; Treatment Outcome

2021

Other Studies

2 other study(ies) available for bicyclol and Liver-Diseases

ArticleYear
Effect of bicyclol on cisplatin-induced hepatotoxicity in the hepatocarcinoma 22 tumour-bearing mice.
    Basic & clinical pharmacology & toxicology, 2009, Volume: 104, Issue:4

    The aim of this study was to determine the effect of bicyclol against cisplatin-induced hepatotoxicity and the influence on the antitumour capacity of cisplatin in hepatocarcinoma 22 (H22) tumour-bearing mice. ICR mice were treated with bicyclol (250 mg/kg, orally) 2 hr before the injection of cisplatin (5 mg/kg, intraperitoneally) for 5 days (once daily) after H22 tumour cells were implanted. All animals were killed on the fifth day after cisplatin treatment and tumour weight of each animal was measured. Liver pathological changes were examined by light microscopy and biochemical assay. The expressions of liver inducible nitric oxide synthase (iNOS and nitric oxide synthase 2) and 3-nitrotyrosine were assessed by Western blotting. Bicyclol showed a significant protection as evidenced by the decrease of elevated serum aminotransferases and lactate dehydrogenase, and improvement of histopathological injury induced by cisplatin. The formation of liver malondialdehyde with a concomitant reduction of reduced glutathione was also inhibited by bicyclol, while the activities of liver superoxide dismutase, catalase and glutathione peroxidase were all increased, respectively. In addition, the over expressions of liver iNOS and 3-nitrotyrosine were suppressed by bicyclol. The administration of bicyclol had no affect on the anti-tumour capacity of cisplatin in mice bearing H22 tumour. The hepatoprotective action of bicyclol provides a new approach for preventing the hepatotoxicity induced by cisplatin in the clinic.

    Topics: Animals; Antineoplastic Agents; Biphenyl Compounds; Blotting, Western; Carcinoma, Hepatocellular; Cell Line, Tumor; Chemical and Drug Induced Liver Injury; Cisplatin; Drug Interactions; Gene Expression Regulation; L-Lactate Dehydrogenase; Liver; Liver Diseases; Liver Neoplasms, Experimental; Male; Mice; Mice, Inbred ICR; Nitric Oxide Synthase Type II; Transaminases; Tyrosine

2009
Effects of bicyclol on liver regeneration after partial hepatectomy in rats.
    Digestive diseases and sciences, 2009, Volume: 54, Issue:4

    Bicyclol is a synthetic antihepatitis drug with antioxidative property. The present study was performed to investigate the effect of bicyclol on liver regeneration after partial hepatectomy in rats. Bicyclol (300 mg/kg) was given to rats subjected to 70% hepatectomy three times before operation. At 6, 24, and 48 h after resection, samples were collected for the measurement of serum alanine aminotransferase (ALT), total bilirubin (TBil), hepatic glycogen, malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH). Moreover, liver regeneration rate, proliferating cell nuclear antigen (PCNA) labeling, proliferation index, and histopathological examination were evaluated at 48 h after hepatectomy. As a result, bicyclol significantly increased regeneration rate, mitotic index (MI), PCNA labeling index, and proliferation index in PH rats. Additionally, bicyclol remarkably inhibited the elevation of serum ALT and TBil levels, alleviated the formation of liver MDA, restored impaired antioxidant SOD and GSH, increased hepatic glycogen content, and also attenuated hepatic vacuolar degeneration. These results suggested that bicyclol had a beneficial effect on liver regenerative capacity of the remnant liver tissue after hepatectomy, probably due to its antioxidative property.

    Topics: Alanine Transaminase; Animals; Bilirubin; Biphenyl Compounds; Cell Proliferation; Glutathione; Glycogen; Hepatectomy; Hepatocytes; Liver; Liver Diseases; Liver Regeneration; Male; Malondialdehyde; Mitotic Index; Proliferating Cell Nuclear Antigen; Rats; Rats, Sprague-Dawley; Superoxide Dismutase

2009