Protective Effect of Vitamin C on Triptolide-induced Acute Hepatotoxicity in Mice through mitigation of oxidative stress

Abstract

Triptolide, a purified diterpenoid from the herb Tripterygium wilfordii Hook.f., was widely used to treat many diseases. However, the hepatotoxicity of triptolide limited its clinical use. Research showed oxidative stress played an important role in triptolide-induced liver injury. To investigate the effect of vitamin C, which was one of the most effective antioxidants, on triptolide-induced hepatotoxicity and its potential mechanism in mice. In the present study, acute liver injury was induced by intraperitoneal injection of triptolide and vitamin C was orally administered. The results showed treatment with vitamin C prevented the triptolide-induced liver injury by reducing the levels of aspartate transaminase from 286.86 to 192.48 U/mL and alanine aminotransferase from 746.75 to 203.36 U/mL. Histopathological changes of liver corresponded to the same trend. Furthermore, vitamin C also protected the liver against triptolideinduced oxidative stress by inhibiting the generation of malondialdehyde (2.22 to 1.49 nmol/mgprot) and hydrogen peroxide (14.74 to 7.19 mmol/gprot) and restoring the level of total superoxide dismutase (24.32 to 42.55 U/mgprot) and glutathione (7.69 to 13.03 μg/mgprot). These results indicated that vitamin C could protect against triptolide-induced liver injury via reducing oxidative stress, and vitamin C may pose a significant health protection in the clinical use of triptolide.

Protection of Bortezomib-induced Neurotoxicity by Antioxidants

“…We also found that antioxidants, VC and NAC effectively neutralized the Bmib-induced neurotoxicity. Since both VC and NAC have been reported to protect cells from the oxidative stress observed in cardiac autonomic neuropathy (15), liver injury (16), ischemia reperfusion injury (17) and critical limb ischemia (18), the oxidative stress may be involved in the present Bmib-induced neurotoxicity. Metabolomics and DNA microarray analysis may provide the evidences of oxidative stress that may be involved in the Bmib-induced neurotoxicity.…”

Procyanidin B1 promotes in vitro maturation of pig oocytes by reducing oxidative stress

“…Accumulation of ROS leads to activation of p53 in cells and antioxidants can reduce ROS levels, preventing the activation of p53 , thereby reducing apoptosis (Gong et al, 2016; Kim et al, 2008). Anti‐oxidants, such as VC, can reduce the expression of the apoptotic marker caspase‐3 during the treatment of certain forms of heart disease, and increase the GSH levels (El‐Shitany & El‐Desoky, 2016; Xu et al, 2019). Decrease in GSH content is a potential early activation signal for apoptosis, and subsequent generation of oxygen free radicals can induce apoptosis (Armstrong et al, 2002).…”

Integrative omics analysis reveals the protective role of vitamin C on perfluorooctanoic acid-induced hepatoxicity

“…Therefore, identifying a supplement for reducing the hepatotoxicity of PFOA can be helpful for the public. Vitamin C, for example, is an antioxidant commonly for boosting liver function [29] , [30] . In this study, we sought to evaluate the possible protective role of vitamin C on PFOA-induced hepatotoxicity using a mouse model.…”

“…In addition, vitamin C supplementation was suggested to provide a protective effect on toxicant-induced hepatotoxicity [15] . Moreover, a study on mice showed that vitamin C retarded triptolide-induced acute hepatotoxicity through oxidative stress mitigation [16] . A similar protective effect of vitamin C was reported for fipronil-induced oxidative stress in mouse liver [16] .…”

“…Moreover, a study on mice showed that vitamin C retarded triptolide-induced acute hepatotoxicity through oxidative stress mitigation [16] . A similar protective effect of vitamin C was reported for fipronil-induced oxidative stress in mouse liver [16] . Furthermore, vitamin C exhibited protective effects on arsenic-induced hepatic anomalies and dexmedetomidine-induced liver injury in rats [18] , [19] .…”