Curcumin, the main active constituent of turmeric (Curcuma longa L.), induces apoptosis in hepatic stellate cells by modulating the abundance of apoptosis-related growth factors.

In order to elucidate the mechanism of action of curcumin against hepatic fibrosis, cultured rat hepatic stellate cells (HSC) (HSC-T6) were incubated with curcumin for 24 h, after which apoptosis was measured by flow-cytometry. The protein levels of the pro-apoptotic factors Fas and p53b as well as of the anti-apoptotic factor Bcl-2 were monitored by immunocytochemical ABC staining after incubation with curcumin for 24 h. In the case of 20 μM curcumin, not only was the respective apoptosis index increased, but also the abundance of the pro-apoptotic factors Fas and p53 were amplified, whereas that of the anti-apoptotic factor Bcl-2 decreased.

Induction of autophagy and apoptosis by miR-148a through the sonic hedgehog signaling pathway in hepatic stellate cells.

Autophagy is an evolutionarily conserved biological process that is activated in response to stress. Increasing evidence indicate that dysregulated miRNAs significantly contribute to autophagy and are thus implicated in various pathological conditions, including hepatic fibrosis. MiR-148a, a member of the miR-148/152 family, has been found to be downregulated in hepatic fibrosis and human hepatocellular carcinoma.

Transforming growth factor‑β1 reduces apoptosis via autophagy activation in hepatic stellate cells.

Autophagy is a metabolic process that is important in fibrogenesis, in which cellular components are degraded by lysosomal machinery. Transforming growth factor β1 (TGF‑β1) is a potent fibrogenic cytokine involved in liver fibrosis; however, it remains elusive whether autophagy is regulated by TGF‑β1 in this process. In the present study, the function of TGF‑β1‑mediated autophagy in the proliferation and apoptosis of hepatic stellate cells (HSCs) was investigated.

[Effects of nerve growth factor on proliferation of hepatic stellate cells].

Objective: To determine the effects of nerve growth factor (NGF) on proliferation of hepatic stellate cells (HSCs) and investigate the related molecular mechanism.

Methods: After incubating cultured HSCs for 24 h with different concentrations of NGF (100, 200 or 400 ng/mL), the cell proliferation was observed by XTT colorimetric assay and cell cycle was detected by flow cytometry. Morphological changes in response to a 24 h exposure to 100 ng/mL NGF were observed by transmission electron microscopy.

Percutaneous endoscopic gastrostomy/jejunostomy combined with percutaneous transhepatic biliary drainage in treating malignant biliary obstruction.

Objective: To investigate the safety and efficacy of percutaneous endoscopic gastrostomy/jejunostomy (PEG/PEJ) combined with percutaneous transhepatic biliary drainage (PTCD) in treating malignant biliary obstruction.

Subjects And Methods: Nine patients (6 males and 3 females, average age 71.3 ± 5.

[Preliminary study on mechanism of therapeutic effect of Huganjiexian decoction on hepatic fibrosis].

Objective: To observe the effects of Huganjiexian decoction on rat hepatic fibrosis and the creation of cytokines.

Methods: Rat hepatic fibrosis was induced by intraperitoneally injection of carbon tetrachloride. At the same time, these rats were treated with different dosages of Huganjiexian decoction.

Curcumin prevents liver fibrosis by inducing apoptosis and suppressing activation of hepatic stellate cells.

This study was designed to investigate the prophylactic effects and the mechanisms of curcumin on liver fibrosis in rats. Liver fibrosis was induced in 72 Sprague Dawley rats by intraperitoneal injection of carbon tetrachloride. Rats were divided into control, liver fibrosis, high, medium, and low dose curcumin (200, 100, and 50 mg kg(-1), respectively), and colchicine (0.

[The study of therapeutic effects of curcumin on hepatic fibrosis and variation of correlated cytokine].

Objective: To investigate therapeutic effects of curcumin on hepatic fibrosis and the variation of correlated cytokine.

Methods: Rat models of hepatic fibrosis were made by carbon tetrachloride. Curcumin of 10, 20, 40 mg per 100 gram weight of rat were given to these rats of curcumin group respectively from ninth week.

[Therapeutic effects of curcumin treatment on hepatic fibrosis].

Objective: To investigate the therapeutic effects and mechanisms of curcumin treatment on hepatic fibrosis.

Methods: A model of hepatic fibrosis was established using carbon tetrachloride intraperitoneal injections in rats. Curcumin was administered to one group of the model rats (curcumin group) and the other rats were used as controls (control group).

[Ultrastructural changes of duodenal mucosas and their significance in patients with liver cirrhosis].

Objective: To investigate the ultrastructural changes of duodenal mucosas and their significance in patients with liver cirrhosis (PLC).

Methods: Endoscopic biopsy duodenal mucosa specimens of 60 PLC and 18 healthy volunteers as controls were obtained. Ultrastructural changes of them were studied with transmission electron microscopy.