Purpose: To investigate the underlying mechanism of hepatic sinusoidal obstruction syndrome (HSOS) induced by Gynura segetum by measuring autophagy in mouse models. Methods: The model group was administered G. segetum (30 g/kg/d) by gavage, while the normal control group was administered an equal volume of saline daily for five weeks. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), hepatic histopathological examinations, and Masson staining were performed to evaluate liver injury. Liver intercellular adhesion molecule-1 (ICAM-1) and P-selectin were evaluated by immunohistochemistry. Hepatocellular apoptosis was assessed using the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. Protein expression levels of autophagy markers were measured using Western blot analysis. Results: Gynura segetum was found to significantly induce liver injury compared with control mice, as evidenced by the increase of serum transaminases, a decrease in triglyceride levels, and histopathological changes in mice. Gynura segetum remarkably induced hepatocellular apoptosis and upregulated the expressions of ICAM-1 and P-selectin and also downregulated the protein expression levels of LC3, Atg12 and cytoplasmic polyadenylation element binding protein. Conclusion: Our results suggested that G. segetum induced liver injury with HSOS, and it was partly due to its ability to impair the autophagy pathway.

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Purpose: To investigate the influence of trichostatin A on nerve cell apoptosis in depressive rats and to explore the probable molecular mechanism of action.Methods: A total of 36 Sprague-Dawley rats weighing 200 - 220 g were divided into sham group (n = 12), model group (n = 12) and trichostatin group (n = 12) by randomization. The protein expressions of phosphorylated cAMP responsive element-binding protein (p-CREB) and BDNF, as well as the mRNA expression levels of B-cell lymphoma-2 (Bcl-2) and caspase-3 in each group of rat hippocampus were determined by Western blotting and quantitative reverse transcription-polymerase chain reaction (qRTPCR), respectively. The apoptosis of nerve cells in the brain tissues of the rats was labeled using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining.Results: Compared with those in the sham group, the degree of sucrose preference decreased markedly, while the immobility time after forced swimming test was extended, and the relative expression levels of p-CREB and BDNF proteins in the hippocampus declined (p < 0.05). The mRNA levels of Bcl-2 and caspase-3 and cell apoptosis rate were increased in the model group (p < 0.05). In comparison with the model group, the trichostatin group exhibited increased sucrose preference degree, shortened immobility time following a forced swimming test, and elevated relative expression levels p-CREB and BDNF proteins in the hippocampus (p < 0.05), but lowered mRNA levels of Bcl-2 and caspase-3 and cell apoptosis rate, displaying statistically significant differences (p < 0.05).Conclusion: Trichostatin A reduces cell apoptosis and ameliorates the depression-like behaviors of rats via the regulation of CREB/BDNF signaling pathway. These findings provide new insights into Trichostatin A for the management of depression.