| Background:Diabetes mellitus macroangiopathy is one of the major causes of death in patients with diabetes, which has complicate pathogenesis and is not yet clear. The traditional Chinese medicine (TCM) has the predominance in preventing and curing the diabetes mellitus macroangiopathy without definite pathogenesis.The pathogenesis of Atherosclerosis (AS) is a complex process that involves vascular endothelial cells injury, macrophage infiltration, lipid accumulation. Apigenin is a plant flavonoid which has various biological activities and pharmacological effects. The protect mechanisms of apigenin in brain repair in ischemic cerebrovascular disease may be associated with promoting angiogenesis, anti-oxidative effects, anti-inflammatory, mitigating brain edema, down-regulating the expression of microglia cell. Whether Apigenin can cure Atherosclerosis or not, currently there is no reports. Study further the pharmacological effects and mechanisms for the further development of apigenin and its clinical application.Purpose:This article investigates the level of RBP4to make the comparisons between such objective indices and TCM syndromes to discuss the features and distribution rules of TCM syndromes.The purpose of study is to investigate the protective effect and mechanism of apigenin on the injury of human umbilical vein endothelial cells (HUVECs) induced by high glucose in vitro, and to provide the basis for the effects of apigenin on treatment and prevention of diabetic angiopathy in the future.Methods:1. Clinical Research:The research methods of the paper involve:We select60cases of Diabetes mellitus macroangiopathy as subjects to be investigated and test the level of rbp4by ELISA.2. Experimental Study:The cultured HUVECs were treated with normal glucose (5.5mmol/L), high glucose (25mmol/L), high glucose+apigenin (25mmol/L glucose+10μmol/L,20μmol/L,40μmol/L) for48 h. Cell apoptosis was assessed by CCK8. The content of ROS, SOD, NO, ICAM-1, VCAM-1, MCP-1were assessed by ELISA. The expression levels of P38MAPK was measured by western blot analysis using specific antibodies. Data were presented as mean±standard deviation (SD) and analysed with SPSS17.0software.Results:1. Clinical Research:The levels of BMI in patients with diabetes mellitus macroangiopathy are all increasing, and there are statistical differences in Qi-Yin deficiency syndrome group and Yin-Yang deficiency syndrome group (P<0.01). The levels of RBP4in patients with diabetes mellitus macroangiopathy are all increasing. Comparing with the group of Extreme Heat due to Deficiency of Yin, the RBP4level of Qi-Yin deficiency syndrome group and Yin-Yang deficiency syndrome group are more increased(P<0.05). there are not significant difference between Qi-Yin deficiency syndrome group and Yin-Yang deficiency syndrome group(P>0.05).2. Experimental Study:High glucose can inhibit HUVECs proliferation and increase the cell apoptosis as well as block the cell cycle in Gl/S phase in a time and dose dependent manner.2. Compared with the control group, level of VCAM-1, MCP-1and ICAM-1was significantly increased in high glucose group; Compared with the high glucose group, level of VCAM-1, MCP-1and ICAM-1was significantly decreased in HG+Apigenin group.3. Compared with the control group, level of ROS was significantly increased in high glucose group;and the level of SOD and NO was significantly decreased; Compared with the high glucose group, level of ROS was significantly decreased in HG+Apigenin group, and the level of SOD and NO was significantly increased.4. Compared with the control group, content of P38was significantly increased in high glucose group; Compared with the high glucose group, content of P38was significantly decreased in HG+Apigenin group.Conclusion:The levels of RBP4in patients with diabetes mellitus macroangiopathy are relevant with Qi deficiency and Yin deficiency and are positively correlated with BMI. Protective effect and mechanism of Apigenin on HUVECs cultured with high glucose may be association with inhibiting the oxidative stress and activating the p38MAPK signal pathway. |
PDF Full Text Request