Beneficial effects of yam on carbon tetrachloride-induced hepatic fibrosis in rats

2010 ◽  
Vol 90 (1) ◽  
pp. 161-167 ◽  
Author(s):  
Yin-Ching Chan ◽  
Shih-Chieh Chang ◽  
Sin-Yie Liu ◽  
Hsin-Ling Yang ◽  
You-Cheng Hseu ◽  
...  
2012 ◽  
Vol 9 (1) ◽  
pp. 16 ◽  
Author(s):  
Hong-Ying Gao ◽  
Guo-Yu Li ◽  
Meng-Meng Lou ◽  
Xiao-Yu Li ◽  
Xiu-Yan Wei ◽  
...  

2020 ◽  
Vol 121 ◽  
pp. 109516 ◽  
Author(s):  
Xiang Huang ◽  
Lihui Wang ◽  
Mingyu Meng ◽  
Shijun Zhang ◽  
Thi Thai Hoa Pham ◽  
...  

2014 ◽  
Vol 568-570 ◽  
pp. 1915-1920
Author(s):  
Ji Hong Zhang ◽  
Meng Qiong Shi ◽  
Hai Bo He ◽  
Cai Hong Bai ◽  
Jun Zhi Wang ◽  
...  

Saponins from Rhizoma Panacis Majoris (SRPM), the bioactive component in Rhizoma Panacis Majoris, have been used extensively as a remedy for liver injury diseases and achieved good clinical efficacy, but the underlying mechanisms remain poorly understood. The goal of our present study was to further confirm SRPM hepatoprotective effect, and evaluate that whether SRPM attenuate oxidative stress and fibrosis in carbon tetrachloride (CCl4)-induced hepatic injury, based on these results, investigate the probable mechanisms involved. At first, the separation and purification of SRPM were studied. And then, in the animal experiment, the male Sprague-Dawley rats were randomly divided into control, model, l-SRPM and h-SRPM group. Hepatic fibrosis model were made according to our previous studies reported. At the same time, the experimental rats were treated respectively with relative drugs, once a day for 8 weeks. Hepatoprotective effects of SRPM were evaluated by liver function, total antioxidant capacity and total-superoxide dismutase, histopathological observations and the hepatic fibrosis relative gene expressions. In the study, we found that SRPM significantly improved liver function, serum antioxidation level, reversed the upregulated α-SMA and TIMP1 mRNA expressions, and further increased the MMP1 mRNA expression. Our studies indicated that SRPM exerted beneficially hepatoprotective effects on the CCl4 induced hepatic fibrosis, mainly enhancing liver tissue antioxidant capacity, reducing the lipid peroxidation of hepatocyte membranes, and then alleviating hepatic fibrosis and hepatic cell death.


Hepatology ◽  
1995 ◽  
Vol 21 (4) ◽  
pp. 1083-1088 ◽  
Author(s):  
Malcolm Mackinnon ◽  
Cindy Clayton ◽  
John Plummer ◽  
Michael Ahern ◽  
Patricia Cmielewski ◽  
...  

2020 ◽  
Vol 18 ◽  
pp. 205873922094263
Author(s):  
Bing Deng ◽  
Detao Tang ◽  
Yong Qiang ◽  
Xiang Zheng

MicroRNA-31 (miR-31) is among the most frequently altered microRNAs in human diseases, and altered expression of miR-31 has been detected in a large variety of diseases types. miR-31 could also regulate a variety of cell functions including hepatic fibrosis. Hepatic stellate cells (HSCs) are regarded as the major cell type involved in hepatic fibrosis. Male BALB/c mice (five mice per group aged 6 weeks) received 200 μL of body weight of carbon tetrachloride (10% CCl4) mixed with olive oil intraperitoneally, and the first dose was doubled. To induce hepatic fibrosis, carbon tetrachloride was injected twice a week for 4, 6, 8, and 10 weeks. Control animals were injected with an equal volume of olive oil at the same time intervals. We found that miR-31 expression and fibrosis-related factors in four hepatic fibrosis stages. However, we noted that inhibition of miR-31 was down-regulated fibrosis-related factor expression in F1–F3 stages, but no F4 stage. Thus, we hypothesize that miR-31 may mediate hepatic fibrosis. In this research, we found that inhibition of miR-31 expression significantly inhibited HSC activation. The biological function of miR-31 during HSC activation might be through targeting hypoxia-inducible factor 1-alpha inhibitor (HIF1AN). Inhibition of miR-31 can reduce the transcription factor activity of hypoxia inducible factor 1 (HIF-1) by targeting the biological effects of HIF1AN with the condition of hypoxia. In later hepatic fibrosis could be rescue combining with inhibition of miR-31 and adding heparin-binding EGF-like growth factor (HBEGF).


2011 ◽  
Vol 92 (1) ◽  
pp. 135-150 ◽  
Author(s):  
Marie-Noële Chobert ◽  
Dominique Couchie ◽  
Agnès Fourcot ◽  
Elie-Serge Zafrani ◽  
Yannick Laperche ◽  
...  

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