Objective:To investigate the protective effect of Epigallocatechin-3-gallate (EGCG) on triptolide (TP)-induced immunological liver injuries, and explore the relevant mechanisms of action. Methods: A total of 40 female C57BL/6 mice were randomly divided into four groups:control group,EGCG group,TP group and TP+EGCG group. The ALT levels in serum was examined by Reitman Frankel method. The activity of hepatic MDA,SOD and GSH was examined by spectrophotometry. HE staining was used to observed the changes of the hepatic histopathology. The hepatic IL-17,IL-6 levels was examined by ELISA and the expression of hepatic TLR4 protein was examined by Western blot. Results:The results showed that serum alanine aminotransaminase ( ALT) levels of TP group were obviously elevated (P<0. 005,vs normal control group) and serum ALT levels were obviously reduced in EGCG treatment group(P<0. 005,vs normal TP group). There were no significantly differences between EGCG group and control group (P>0. 05). Meanwhile,EGCG could ameliorate hepatic pathological damage. Furthermore,in TP group,the activity of malondialdehyde ( MDA) ,the expression of Toll-like receptor 4 (TLR4) protein and the contentration of hepatic interleukin (IL)-17,IL-6 were higher than normal control group ( P<0. 005 ) . On the contrary, the activity of superoxide dismutase ( SOD ) and restored glutathione ( GSH ) were significantly lower than normal control group ( SOD, P<0. 05;GSH, P<0. 005 ) . In EGCG treatment group, the expression of TLR4 protein and the concentration of MDA,hepatic IL-17 and IL-6 were lower than TP group ( TLR4,P<0. 05;MDA,P<0. 005;IL-17,P<0. 005;IL-6,P<0. 005). On the contrary,SOD and GSH were significantly higher than TP group (SOD,P<0. 05;GSH,P<0. 005). Conclusion:This study suggests that EGCG possesses hepatoprotective effect against TP-induced immunological liver injury through its anti-inflammatory and anti-oxidant actions.

Objective: To observe the regeneration of palatal fracture in patients with unilateral complete cleft lip and palate. Methods: A total of 35 patients with unilateral complete cleft lip and palate were randomly included as the observation group and 20 with normal teeth as the control group. All the subjects underwent CT with high resolution. Based on the formation of bone bridge, the observation group was further divided into bone bridge formation group and non-bone bridge formation group. The regenerated bone of the bone bridge was measured. The width of the anterior segment, middle segment and posterior segment of the dental arch were measured and statistically analyzed between the observation group and the control group. Results: ①A total of 25 cases with varying degrees of regenerated bone was interconnected to form bone bridge in palatal process, while in the remaining 10 cases, bone was regenerated, but not connected to form bone bridge. ②The width of the middle section of the arch in the observation group was greater than that in the non-bone bridge formation group. The width of each segment in the observation group was less than that in the control group. Conclusions Bone was regenerated to various extent in the palate after cleft palate. The formation of bone bridge is beneficial to the development of dental arch.

Atherosclerosis is a vascular disease characterized by arterial occlusion formed by the pathological accumulation of pathological vascular cells and apoptotic cell debris. Atherosclerotic vulnerable plaque is an important pathological basis for inducing severe thrombotic cardiovascular events， and the study of its etiology and pathogenesis has always been a hot issue in the field of cardiovascular research. Efferocytosis is a new type of programmed death cell removal， which refers to the process of macrophages phagocytosing and degrading apoptotic cells to prevent secondary necrosis. It is a key homeostatic mechanism in the body's physiological process. In the pathological state， the dysfunction of efferocytosis causes the pathological accumulation of apoptotic cells and necrotic debris， leading to the occurrence of secondary cell necrosis and the continuous release of intracellular toxic content and inducing inflammatory regression disorders and cholesterol metabolism disorders， which are closely related to the occurrence and development of atherosclerotic vulnerable plaques. The theory of ''blood stasis and toxin'' is an important theory of traditional Chinese medicine （TCM） to explain the occurrence and development of atherosclerosis. Atherosclerosis starts from the pathological state of blood stagnation. Prolonged blood stagnation leads to blood stasis and toxic substances. Blood stasis and toxic pathogens interact with each other in blood vessels and eventually form plaques in blood vessels. The theory of ''blood stasis and toxin causing a catastrophe'' is an important understanding of the occurrence and development of acute cardiovascular events. From the perspective of TCM theory， the pathophysiological mechanism of efferocytosis is similar to the etiology and pathogenesis of the ''blood stasis and toxin'' in TCM. Therefore， this paper took the theory of ''blood stasis and toxin'' as the breakthrough point to explore the mechanism of efferocytosis in atherosclerotic vulnerable plaques， and proposed a detoxification and blood circulation method to regulate cell burial to prevent and treat atherosclerotic vulnerable plaques. The research strategy aims to provide new ideas and theoretical basis for the prevention and treatment of atherosclerosis by detoxification and blood circulation.

Gliomas are the most common primary intracranial neoplasms among all brain malignancies, and the microtubule affinity regulating kinases (MARKs) have become potential drug targets for glioma. Here, we report a novel dual small-molecule inhibitor of MARK3 and MARK4, designated as PCC0208017. PCC0208017 strongly inhibited kinase activity against MARK3 and MARK4, and strongly reduced proliferation in three glioma cell lines. This compound attenuated glioma cell migration, glioma cell invasion, and angiogenesis. Molecular mechanism studies revealed that PCC0208017 decreased the phosphorylation of Tau, disrupted microtubule dynamics, and induced a G2/M phase cell cycle arrest. In an glioma model, PCC0208017 showed robust anti-tumor activity, blood-brain barrier permeability, and a good oral pharmacokinetic profile. Molecular docking studies showed that PCC0208017 exhibited high binding affinity to MARK3 and MARK4. Taken together, our study describes for the first time that PCC0208017, a novel MARK3/MARK4 inhibitor, might be a promising lead compound for treatment of glioma.