Objective To investigate the effects of Jiawei Danshen Decoction on endothelial cell ultrastructure, serum NO and ET in apolipoprotein E-knockout atherosclerosis (AS) mice;To discuss its mechanism of anti-atherosclerosis.Methods Totally 24 7-8 weeks old ApoE -/- mice were fed with a high fat diet for 12 weeks until the a mature atherosclerotic plaque was formed. They were randomly divided into four groups:model group, control group,Jiawei Danshen Decoction of low-dose group and high-dose group, 6 mice in each group. Another 6 normal C57BL/6J mice with the same strain were set as the blank group, and fed with general diet. After medicine intervention by gavage for 8 weeks, blood was extracted from orbital venous to measure serum NO and ET;aortic endothelial cell ultrastructure changes were observed by transmission electron microscope.Results Compared with the blank group, the level of NO obviously decreased and ET significantly increased in the model group (P<0.01). Compared with model group, medicine intervention increased NO and reduce ET level (P<0.05). Electron microscopy results showed that the model group showed fatty streaks stage performance;endothelial damage in each administration group was improved compared with model group.Conclusion Jiawei Danshen Decoction can improve the endothelial cell ultrastructure and functions and protect endothelial cells, with a purpose to delay the AS process.

Interleukin-27 (IL-27), a heterodimeric cytokine, plays a protective role in diabetes. Ghrelin, a gastric hormone, provides a hunger signal to the central nervous system to stimulate food intake. The relationship between IL-27 and ghrelin is still unexplored. Here we investigated that signal transducer and activator of transcription 3 (STAT3)-mechanistic target of rapamycin (mTOR) signaling mediates the suppression of ghrelin induced by IL-27. Co-localization of interleukin 27 receptor subunit alpha (WSX-1) and ghrelin was observed in mouse and human gastric mucosa. Intracerebroventricular injection of IL-27 markedly suppressed ghrelin synthesis and secretion while stimulating STAT3-mTOR signaling in both C57BL/6J mice and high-fat diet-induced-obese mice. IL-27 inhibited the production of ghrelin in mHypoE-N42 cells. Inhibition of mTOR activity induced by siRNA or rapamycin blocked the suppression of ghrelin production induced by IL-27 in mHypoE-N42 cells. siRNA also abolished the inhibitory effect of IL-27 on ghrelin. IL-27 increased the interaction between STAT3 and mTOR in mHypoE-N42 cells. In conclusion, IL-27 suppresses ghrelin production through the STAT3-mTOR dependent mechanism.

Exosomes (EXOs) are formed by intracellular multivesicular bodies and carry a variety of biomacromolecules such as lipids, proteins, encoding and non-coding RNAs, and mitochondrial DNA. EXOs can be released in vivo by different cell types, including hepatocytes, hepatic stellate cells, and immune cells and play the role of intercellular communication. More and more studies have shown that EXOs are involved in the development, progression, and prognosis of chronic hepatitis B (CHB) and hepatocellular carcinoma (HCC) caused by hepatitis B virus (HBV) infection and are expected to become potential biomarkers for the early diagnosis and prognostic evaluation of HBV-related HCC. This article reviews the role of EXOs in the host infection process of HBV and the importance of EXOs in the development, progression, and prognosis of CHB and HCC, in order to provide new ideas for the basic and clinical research in this field.