Research progress on the relationship between liver cirrhosis and thyroid hormones / 中华肝脏病杂志

There exists a complex relationship between liver and thyroid hormones. Liver plays an important role in the activation, inactivation, transportation, and metabolism of thyroid hormones. At the same time, thyroid hormones also affect hepatocytes activity and liver metabolism, such as lipid and bilirubin metabolism. Importantly, thyroid hormone levels often change abnormally in patients with liver cirrhosis. Therefore, studying the change of thyroid hormone levels in patients with liver cirrhosis has a certain clinical value for assessing the severity, prognosis, diagnosis and treatment. This paper reviews the research progress on the relationship between liver cirrhosis and thyroid hormone.

Effects of nerve growth factor on proliferation of hepatic stellate cells / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To determine the effects of nerve growth factor (NGF) on proliferation of hepatic stellate cells (HSCs) and investigate the related molecular mechanism.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>NGF significantly inhibited HSC proliferation (P less than 0.05) in a dose-independent manner. The optical densities of the XTT colorimetric assay were 0.66+/-0.03 for 100 ng/mL NGF, 0.69+/-0.03 for 200 ng/mL NGF, and 0.66+/-0.03 for 400 ng/mL NGF, all of which were significantly lower than that of the control group (0.73+/-0.01; P less than 0.05). All concentrations of NGF led to significantly higher numbers of HSCs in the G2 phase (100 ng/mL: 14.83+/-5.41%, 200 ng/mL: 14.73+/-2.50%, and 400 ng/mL: 14.87+/-2.06%), compared to that detected in the control group (7.47+/-4.39%; P less than 0.05). Twenty-four hours of exposure to 100 ng/mL NGF caused morphological changes indicative of apoptosis.</p><p><b>CONCLUSION</b>NGF inhibits the proliferation of HSCs, possibly by arresting the cells in the G2 phase of the cell cycle. NGF-inhibited cells may also undergo apoptosis.</p>

Preliminary study on mechanism of therapeutic effect of Huganjiexian decoction on hepatic fibrosis / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To observe the effects of Huganjiexian decoction on rat hepatic fibrosis and the creation of cytokines.</p><p><b>METHODS</b>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. Sho-saiko-to compound treating group and Fufangbiejiarangan Tablets treating group were used as positive controls. After twelve weeks, all rats were executed. Histopathologic changes were observed after H.E and Masson stainings. The expression of collagen type I, collagen type III, TGF-beta 1 and PDGF-BB in liver were detected by immunohistochemical staining.</p><p><b>RESULTS</b>Compared with fibrotic group, hepatic fibrosis in decoction groups was significantly improved. In decoction groups, levels of collagen type I, collagen type III, TGFbeta1 and PDGF-BB were decreased, especially in the low-dose curcumin group. The TGF-beta 1 positive percentage were 7.56%+/-2.18%, 29.25%+/-7.84%, 13.54%+/-4.15%, 21.82%+/-6.64%, 20.06%+/-7.14%, 13.78%+/-4.35%, 12.75%+/-3.98% in liver tissues from normal group, model group, low, middle, high curcumin, Sho-saiko-to compound and Fufangbiejiarangan Tablets treating groups respectively (P less than 0.05); while the PDGF-BB positive percentage were 1.68%+/-0.41%, 11.70%+/-2.28%, 3.65%+/-0.76%, 5.24%+/-1.04%, 6.37%+/-1.12%, 4.16%+/-0.61%, 3.38%+/-0.56% in liver tissues from those groups respectively (P less than 0.05).</p><p><b>CONCLUSION</b>Huganjiexian decoction can improve rat hepatic fibrosis, possibly via inhibiting the expression of collagen type I, collagen type III, TGFbeta1 and PDGF-BB.</p>

The role and mechanisms of cyclooxygenase-2 inhibitors on the proliferation of hepatic stellate cell / 中华肝脏病杂志

<p><b>OBJECTIVES</b>To observe the effects of NS-398 on proliferation of hepatic stellate cells (HSCs) in vitro, and to investigate the possible molecule mechanism.</p><p><b>METHODS</b>HSCs were incubated with different concentrations of NS-398. The effects of NS-398 on cell proliferation was detected by MTT colormetric assay. The cell cycle of HSCs was analyzed by Flow Cytometry (FCM), cyclooxygenase-2 (COX-2) and proliferating cell nuclear antigen (PCNA) proteins in HSCs were detected by immunocytochemistry.</p><p><b>RESULTS</b>Administration of 20-160 micromol/L NS-398 significantly inhibited HSCs proliferation in dose-dependent manner compared with the control group (P less than 0.01). After treated with NS-398 at concentrations of 90, 120, and 150 micromol/L for 48 h, the number of HSCs in G(2)/M phase increased and the number of HSCs in G(0)/G(1) phase decreased (P less than 0.05); Incubated with 120 micromol/L NS-398 for 48 h, percentage of masculine cell of PCNA was 28.91%+/-0.11%, which was significantly lower than that of the control group (85.99%+/-0.13%) (P less than 0.01). Percentage of masculine cell of COX-2 was 13.80%+/-0.43%, which was not significantly different from that of the control group (14.07%+/-0.59%) (P more than 0.05).</p><p><b>CONCLUSIONS</b>NS-398 could inhibit the proliferation of HSC-T6 and arrest HSCs in G2/M phase. Down-regulation of PCNA protein may partially accounted for the proliferation inhibition effect on HSCs induced by NS-398.</p>

Prophylactic effect of curcumin on hepatic fibrosis and its relationship with activated hepatic stellate cells / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To observe the prophylactic effect of curcumin on hepatic fibrosis and the number, location, apoptosis of activated hepatic stellate cells (HSCs) in the livers and to discuss the relationship between the prophylactic effects and activated HSC.</p><p><b>METHODS</b>A rat model of hepatic fibrosis was established by intraperitoneal injection of carbon tetrachloride. Curcumin doses of 5 mg, 10 mg, 20 mg per 100 gram per 100g of body weight were given to three groups of the model rats. No curcumin was given to one group of the model rats and it served as the control. After eight weeks, all rats were sacrificed and their left liver lobes were examined histopathologically with H.E and Masson stainings. Grades of hepatic fibrosis were evaluated according to the SSS system. Activated HSC was detected by the alpha-SMA immunohistochemistry staining. HSC apoptosis was detected by double-stainings of terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) and desmin immunohistochemistry staining.</p><p><b>RESULTS</b>Degrees (SSS system scores) of hepatic fibrosis in the curcumin groups were all less severe in comparison with those of the control group. Activated HSCs in the livers of the rats of the control group increased significantly compared with that of the treatment groups, and also fewer apoptotic HSCs were detected in the control group. On the contrary, fewer activated HSCs and more apoptotic HSCs were detected in the curcumin groups compared with those of the control group. The degrees of the effects were curcumin dose-dependent.</p><p><b>CONCLUSIONS</b>Curcumin can prevent hepatic fibrosis. It can inhibit activation and proliferation of HSCs and induce HSCs apoptosis, which may be the mechanism(s) contributing to the prophylactic effects of curcumin on hepatic fibrosis.</p>