Protective Effect of 18<i>β</i>‐Glycyrrhetinic Acid against Triptolide‐Induced Hepatotoxicity in Rats

Yang, Guanghua; Wang, Lan; Yu, Xiu-Ting; Huang, Yanfeng; Qu, Chang; Zhang, Zhenbiao; Luo, Dandan; Lin, Ji; Zhou, Lian; Su, Zi-Ren; Zhang, Xiaojun; Chen, Haiming

doi:10.1155/2017/3470320

Cited by 16 publications

(21 citation statements)

References 37 publications

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“…Unfortunately, their application has been increasingly restricted due to their potential adverse effects and acute toxicity, particularly hepatic toxicity. To date, various studies have been performed with the aim of identifying strategies to reduce the side effects of these agents ( 24 – 26 ). However, counteractive therapeutic approaches against TP-induced hepatotoxicity are yet to be established.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of silymarin on triptolide-induced acute hepatotoxicity in rats

Wang

Huang

et al. 2017

Mol Med Report

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Silymarin has been used in the treatment of a number of liver diseases for a long time, but its efficacy in preventing triptolide induced acute hepatotoxicity has not been reported previously. The present study aimed to assess the protective effect of silymarin against triptolide (TP)-induced hepatotoxicity in rats. Rats were orally administrated with silymarin (50, 100 and 200 mg/kg) for 7 days and received intraperitoneal TP (2 mg/kg) on the day 8. Hepatic injuries were comprehensively evaluated in terms of serum parameters, morphological changes, oxidative damage, inflammation and apoptosis. The results demonstrated that TP-induced increases in serum parameters, including alanine transaminase, aspartate aminotransferase, alkaline phosphatase, total cholesterol and γ-glutamyl transpeptidase, which were determined using a biochemical analyzer, and histopathological alterations and hepatocyte apoptosis as determined by hematoxylin and eosin and TUNEL staining, respectively, were prevented by silymarin pretreatment in a dose-dependent manner. TP-induced depletions in the activity of the antioxidant enzymes superoxide dismutase, glutathione peroxidase, glutathione S-transferase and catalase, and glutathione levels, were also significantly reversed by silymarin, as determined using specific kits. Additionally, silymarin dose-dependently exhibited inhibitory effects on malonaldehyde content in the liver. The production of proinflammatory cytokines was investigated using ELISA kits, and the results demonstrated that silymarin dose-dependently inhibited the production of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-10 and IL-1β in the liver. To determine the mechanism of silymarin, western blot analysis was performed to investigate the protein expression of phosphorylated (p)-p38 and p-c-Jun N-terminal kinase (JNK) of the TNF-α induced inflammatory response and apoptotic pathways. Silymarin significantly blocked p38 and JNK phosphorylation and activation. Additionally, the expression of the proapoptotic proteins cytochrome c, cleaved caspase-3 and Bcl-2-associated X was also reduced following treatment with silymarin, as determined by ELISA, western blotting and immunohistochemistry, respectively. In conclusion, silymarin was demonstrated to dose-dependently protect rat liver from TP-induced acute hepatotoxicity, with the high dose (200 mg/kg) achieving a superior effect. This protective effect may be associated with the improvement of antioxidant and anti-inflammatory status, as well as the prevention of hepatocyte apoptosis. Therefore, silymarin may have the potential to be applied clinically to prevent TP-induced acute hepatotoxicity.

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Section: Discussionmentioning

confidence: 99%

Protective effects of silymarin on triptolide-induced acute hepatotoxicity in rats

Wang

Huang

et al. 2017

Mol Med Report

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“…In this study, the adverse events in the TwHF group were much lower than those in the glucocorticoid group (13 vs 19), and most adverse events in TwHF were mild and controllable. Other adverse reactions regarding TwHF, which have been reported in the literature were not noticed in our study, such as skin rashes, pigmentation, and genital dysfunction 14 . In this study, because the average age of patients was 78 years of age, this dose of more than 60 mg/day was not used on our patients.…”

Section: Discussionmentioning

confidence: 63%

Treatment of bullous pemphigoid in Chinese patients withTripterygium wilfordiiHook F

Jin

et al. 2020

Dermatologic Therapy

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Tripterygium wilfordii Hook F (TwHF) is a traditional Chinese herb used in many medicinal applications, but the treatment of bullous pemphigoid (BP) with TwHF has never been reported. The aim of this study was to evaluate the efficacy and safety of TwHF in BP patients. A retrospective study was performed from January 2015 to September 2019 in the Department of Dermatology, Peking Union Medical College Hospital. A total of 10 patients with mild to moderate BP and treated with TwHF were enrolled in the study with 10 mild or moderate BP patients treated with systemic glucocorticoid randomly selected as controls. In the TwHF group, a major response was seen in seven patients, a minor response in one and no response was seen in two patients. In the glucocorticoid group, a major response was seen in nine patients and a minor response in one patient. Two patients experienced treatment failure. The time to disease control in the TwHF group (34 ± 11 days) was longer as compared to the glucocorticoid group (18 ± 8 days, P < .05). Ten patients relapsed during the follow‐up period. The adverse events in the TwHF group were lower than those in the glucocorticoid group (13 vs 19). Low‐dose TwHF may be effective and safe for treating mild and moderate BP.

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“…These findings suggest that GA may serve as a novel chemotherapeutic potential for treating pituitary adenoma and deserves further clinical research. Previous studies demonstrated the protection of low-dose GA (50 mg/kg) against TP-induced hepatotoxicity in rats, which may mediate via anti-inflammation, antioxidation, and antiapoptosis (Yang et al, 2017[ 30 ]). In addition, the protective effect is dose-related, which is only mediated by low-dose GA (50 mg/kg), but not high-dose GA (100 mg/kg) (Yang et al, 2017[ 30 ]).…”

Section: Discussionmentioning

confidence: 99%

18 beta-glycyrrhetinic acid ameliorates the cognitive functions and decreases the recurrence rate of pituitary adenomas patients

Wang

Zhang

Xiao

et al. 2018

EXCLI Journal; 17:Doc753; ISSN 1611-2156

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Protective Effect of 18β‐Glycyrrhetinic Acid against Triptolide‐Induced Hepatotoxicity in Rats

Cited by 16 publications

References 37 publications

Protective effects of silymarin on triptolide-induced acute hepatotoxicity in rats

Protective effects of silymarin on triptolide-induced acute hepatotoxicity in rats

Treatment of bullous pemphigoid in Chinese patients withTripterygium wilfordiiHook F

18 beta-glycyrrhetinic acid ameliorates the cognitive functions and decreases the recurrence rate of pituitary adenomas patients

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