Hepatoprotective effects of ethyl pyruvate against CCl4-induced hepatic fibrosis via inhibition of TLR4/NF-?B signaling and up-regulation of MMPs/TIMPs ratio - 21/02/18
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| Iconografías | 5 |
| Vídeos | 0 |
| Otros | 0 |
Highlights |
• | We make the CCl4-induced hepatic fibrosis model and intervene with EP. |
• | EP improves CCl4-induced hepatic morphological change and liver function. |
• | EP could regulate the ratio of MMPs to TIMPs and inhibit HSC activation. |
• | CCl4-induced TLR4/NF-κB signal activation is antagonized by EP. |
• | EP can serve as complementary and alternative treatment to protect hepatic fibrosis. |
Summary |
Background and aim |
Liver fibrosis is a worldwide clinical issue. It has been well established that liver fibrosis is characterized of excessive extracellular matrix (ECM) deposition in chronically damaged livers. Accumulating evidences have suggested that ethyl pyruvate (EP) is a potential useful agent for preventing from hepatic injury. The aim of this study was to evaluate the protective effects of the EP against liver fibrosis induced by carbon tetrachloride (CCl4) in rats.
Method |
Rats were randomly divided into control group, CCl4 group and CCl4+EP group, which with and without EP administration. Liver fibrosis was evaluated by serum biochemical parameters levels, Masson's trichromic staining and immunohistochemistry. Q-RTPCR was used to indicate genes expression. ELISA was used to detect proteins level.
Results |
This study demonstrates that Toll-like receptors 4 (TLR4)/nuclear factor kappa B (NF-κB) signal is an important regulator of liver fibrosis while TLR4/NF-κB mRNA and protein levels reduced during HSCs activation. In addition, down-regulated high-mobility group box 1 (HMGB1) expression reduced NF-κB transcription and phosphorylation, which inhibited HSCs activation by blocking the TLR4 signal. Moreover, EP contributed to an increase in the ratio of matrix metalloproteinase (MMPs) to tissue inhibitor of matrix metalloproteinase (TIMPs), which might facilitate the degradation of the ECM. In CCl4-induced liver fibrosis rats, additional EP injection resulted in decreased ECM deposition and improved liver function.
Conclusion |
In conclusion, the present findings indicated that EP might be an effective agent for anti-fibrotic therapy.
El texto completo de este artículo está disponible en PDF.Keywords : Hepatic fibrosis, Ethyl pyruvate, Matrix metalloproteinase, Tissue inhibitor of matrix metalloproteinase
Esquema
Vol 42 - N° 1
P. 72-81 - février 2018 Regresar al número
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