Potential protection of vitamin C against liver-lesioned mice

Su, Min; Chen, Hongqiu; Wei, Chaohe; Chen, Ning; Wu, Wei

doi:10.1016/j.intimp.2014.07.034

Cited by 23 publications

(19 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Coadministration of vitamin C and nicotine significantly decreased liver enzymes ALT, AST, and ALP compared to nicotine treated group. This result is supported by the work of Su and his colleague who reported a hepatoprotective effect of vitamin C against carbon tetrachloride-induced liver damage and elevation of liver enzymes [35]. Moreover, this study showed that vitamin C supplementation decreased the degree of hepatocyte injury and vacuolation of its cytoplasm.…”

Section: Discussionsupporting

confidence: 75%

Protective Effects of Vitamin C against Nicotine-Induced Oxidative Damage of Rat Liver and Kidney

Mahmoud¹

2014

IOSRJESTFT

View full text Add to dashboard Cite

Abstract:Objective: Vitamin Methods: Animals were divided into four groups; (C) saline-treated, (VC) vitamin C-treated, (NIC) nicotinetreated, all were for 3 weeks, and (NIC+VC) is given vitamin C for 3 days prior, with nicotine injection and 2 days thereafter. Results: Present work showed that nicotine exposure caused significant reduction in total body weight, relative liver and kidney weights, elevated malondialdehyde (MDA), alanine transaminase (ALT), aspirate transaminase (AST), and alkaline phosphatase (ALP) in both hepatic and renal tissues. Co-exposure to nicotine and vitamin C maintained normal liver and kidney weight, significantly lowered MDA, ALT, AST, ALP and elevated glutathione in both hepatic and renal tissues compared NIC group as well as controls. Nicotine administration resulted in shedding, necrosis, and loss of brush border of cells covering proximal and distal convoluted tubules of kidney. The liver in the nicotine-treated group showed vacuolated cytoplasm of hepatocytes, with dilated central vein and sinusoids and mitochondrial destruction. Immunohistochemistry showed dense PCNA immunostaining in the livers of nicotine-treated rats. Vitamin C induced partial correction of nicotine-induced histopathological damage of liver and kidney and significant elevation in PCNA expression. Conclusion:The results of present work suggested that vitamin C has a promising prophylactic effect against nicotine-induced oxidative damage of liver and kidney.

show abstract

Section: Discussionsupporting

confidence: 75%

Protective Effects of Vitamin C against Nicotine-Induced Oxidative Damage of Rat Liver and Kidney

Mahmoud¹

2014

IOSRJESTFT

View full text Add to dashboard Cite

show abstract

“…Fifth, we used vitamin C as the control rather than a placebo. Previous reports have shown the potential effects of vitamin C in anti-hepatotoxicity, 34 which may lower the preventive effect of silymarin in ATLI. Vitamin C is inexpensive and easy to access.…”

Section: Discussionmentioning

confidence: 99%

Preventive use of a hepatoprotectant against anti‐tuberculosis drug‐induced liver injury: A randomized controlled trial

Zhang

Pan²,

Peng

et al. 2016

J of Gastro and Hepatol

View full text Add to dashboard Cite

Background and Aim: Hepatoprotectants are routinely prescribed in China to prevent anti-tuberculosis drug-induced liver injury (ATLI). However, their biological mechanismshave not yet been clearly demonstrated. This study aims to evaluate the preventive effects of Silybum marianum against drug-induced liver injury among tuberculosis patients and to provide clinical guidelines for tuberculosis management in China. Methods: A randomized controlled trial was performed in Jiangsu, China. Tuberculosis patients were randomly allocated to the experimental group (anti-tuberculosis therapy plus S. marianum capsule) or the control group (anti-tuberculosis therapy plus vitamin C tablet). The primary outcomes were the occurrence of probable and possible ATLI, the peak aspartate aminotransferase/alanine aminotransferase ratio and the maximum altered alkaline phosphatase or gamma-glutamyl transferase.Results: The final analysis comprised 183 cases in the experiment group and 187 cases in the control group. The risk of developing probable ATLI was not significantly different between the two groups. During the follow-up period, 43.72% of cases in the experiment group and 35.83% of cases in the control group were determined to have possible ATLI (relative risk = 1.23, 95% confidence interval: 0.94-1.54). When using a more strict definition of possible ATLI, the adjusted relative risk (95% confidence interval) was 1.76 (1.14-2.56). The risks of adverse drug reactions, prolonged treatment length, taking second-line tuberculosis drugs, and the clearance of tuberculosis bacteria were similar between the two groups. Conclusions: No significant preventive effect of silymarin was found for either lowering the risk of liver injury or boosting the positive outcomes. Worse, we even found a potential risk of liver damage caused by the hepatoprotectant.

show abstract

“…Moreover, buildup of NF-κB in liver cells can result in the recruitment of inflammatory cytokines/mediators, thus inducing fibrosis development [30]. TLR-4 exhibits a fundamental role in managing innate immunity activation and regulates the recruitment of cytokines that are necessary for the progression of inflammation [31,32]. Previous studies have found that high levels of TLR4 in the liver are implicated in inflammatory formation, thereby participating in fibrosis [33].…”

Section: Discussionmentioning

confidence: 99%

Anti-Fibrotic Effect of Plumbagin on CCl4-Lesioned Rats

Wei

Huang

Liu

et al. 2015

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Our previous studies have shown that plumbagin effectively inhibits hepatic stellate cell (HSC) proliferation. Thus, plumbagin-mediated anti-fibrotic effects in vivo merit further investigation. Methods: We used rat models to assess the potential benefits of plumbagin against CCl₄-induced liver fibrosis. Results: The results showed that plumbagin lowered the serum concentrations of liver functional enzymes (ALT, AST, ALB, TBIL) in CCl₄-fibrotic rats while reducing inflammatory cytokine levels (IL-6, TNF-a). As reflected in pathological examinations, rats that were administered plumbagin showed decreased collagen markers (HA, LN, PCIII and CIV) in liver tissues and improved hepatocellular impairments. In addition, plumbagin contributed to down-regulating NF-κB and TLR-4 mRNA in CCl₄-lesioned livers. As revealed in the immunohistochemical assay, plumbagin-administered rats showed reduced levels of a-SMA and TNF-a immunoreactive cells in liver tissue. Conclusion: Collectively, these findings offer appealing evidence that plumbagin may serve as an anti-fibrotic medication through inactivating the NF-κB/TLR-4 pathway that is associated with inflammatory reactions, thereby mitigating liver fibrosis.

show abstract

Potential protection of vitamin C against liver-lesioned mice

Cited by 23 publications

References 18 publications

Protective Effects of Vitamin C against Nicotine-Induced Oxidative Damage of Rat Liver and Kidney

Protective Effects of Vitamin C against Nicotine-Induced Oxidative Damage of Rat Liver and Kidney

Preventive use of a hepatoprotectant against anti‐tuberculosis drug‐induced liver injury: A randomized controlled trial

Anti-Fibrotic Effect of Plumbagin on CCl4-Lesioned Rats

Contact Info

Product

Resources

About