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The Dimethylnitrosamine Induced Liver Fibrosis Model in the Rat
Published on: June 17, 2016
Neferine Exerts Antioxidant and Anti-Inflammatory Effects on Carbon Tetrachloride-Induced Liver Fibrosis by
Yuanyuan Wang1, Shaozhan Wang1, Rong Wang1
1Department of Pharmacy, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhi Zao Ju Rd, Shanghai 200011, China.
Abstract:
Reversible liver fibrosis is the consequence of diverse liver injuries. Oxidative stress combined with inflammation is the primary cause of carbon tetrachloride- (CCl4-) induced liver fibrosis. Neferine is a bibenzyl isoquinoline alkaloid, which has strong anti-inflammatory and antioxidant properties. The present study attempted to find its antiliver fibrosis effect and explore the potential mechanism to relieve oxidative stress and inflammation in rats with CCl4-induced liver fibrosis. Herein, we found that neferine noticeably mitigated fibrosis and improved liver function. Furthermore, neferine increased the activity of antioxidant enzymes, such as superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and catalase (CAT), but decreased the level of malondialdehyde (MDA). Neferine also decreased the levels of alpha-smooth muscle actin (α-SMA), transforming growth factor β1 (TGF-β1), and inflammatory factors. These results may demonstrate that neferine could effectively inhibit oxidative stress and inflammation in liver fibrosis. To account for the potential mechanism by which neferine relieves oxidative stress and inflammation in liver fibrosis rats, immunohistochemistry analyses and western blotting were performed. The results showed that neferine inhibited the mitogen-activated protein kinase (MAPK) pathway, as evidenced by the reduced phosphorylation of p38 MAPK, ERK 1/2, and JNK. And it inhibited the nuclear factor- (NF-) κB/IκBα pathway, as evidenced by preventing the translocation of NF-κB into nuclei. Our findings indicated a protective role for neferine, acting as an antioxidant and anti-inflammatory agent in CCl4-induced liver fibrosis.
Insights
Neferine effectively combats liver fibrosis by reducing oxidative stress and inflammation. This natural compound protects liver function and mitigates fibrosis through antioxidant and anti-inflammatory pathways.
Area of Science:
- Pharmacology and Toxicology
- Hepatology
- Natural Product Chemistry
Background:
- Liver fibrosis, a reversible condition from liver injury, is primarily driven by oxidative stress and inflammation, particularly in carbon tetrachloride (CCl4)-induced models.
- Neferine, a bibenzyl isoquinoline alkaloid, possesses known anti-inflammatory and antioxidant properties, suggesting potential therapeutic applications.
- Understanding the mechanisms by which neferine impacts liver fibrosis is crucial for developing novel treatments.
Purpose of the Study:
- To evaluate the anti-fibrotic effects of neferine in a rat model of carbon tetrachloride (CCl4)-induced liver fibrosis.
- To investigate the underlying mechanisms through which neferine alleviates oxidative stress and inflammation in the context of liver fibrosis.
- To explore neferine's impact on key molecular pathways involved in fibrogenesis and inflammatory responses.
Main Methods:
- Induction of liver fibrosis in rats using carbon tetrachloride (CCl4).
- Administration of neferine and assessment of liver function and fibrosis markers.
- Measurement of antioxidant enzyme activities (SOD, GSH-PX, CAT) and lipid peroxidation (MDA).
- Analysis of fibrotic markers (α-SMA, TGF-β1) and inflammatory factors.
- Investigation of signaling pathways (MAPK, NF-κB) using immunohistochemistry and Western blotting.
Main Results:
- Neferine treatment significantly mitigated liver fibrosis and improved overall liver function in CCl4-treated rats.
- Neferine administration increased the activity of antioxidant enzymes (SOD, GSH-PX, CAT) and decreased malondialdehyde (MDA) levels, indicating reduced oxidative stress.
- Neferine effectively reduced the expression of α-SMA, TGF-β1, and key inflammatory factors.
- Neferine inhibited the MAPK pathway by reducing the phosphorylation of p38 MAPK, ERK 1/2, and JNK.
- Neferine suppressed the NF-κB/IκBα pathway by preventing the nuclear translocation of NF-κB.
Conclusions:
- Neferine demonstrates significant protective effects against CCl4-induced liver fibrosis in rats.
- Neferine functions as a potent antioxidant and anti-inflammatory agent, ameliorating liver damage.
- The therapeutic benefits of neferine are mediated through the inhibition of oxidative stress, inflammation, and key fibrogenic signaling pathways, including MAPK and NF-κB.
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