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ObjectiveTo explore the therapeutic effect and mechanism of Guipitang on rats with myocardial ischemia. MethodFifty SD rats were divided into five groups： a control group， a model group， low and high-dose Guipitang （7.52， 15.04 g·kg-1） groups， and a trimetazidine group （0.002 g·kg-1）. By intragastric administration of vitamin D3 and feeding rats with high-fat forage and injecting isoproterenol， the rat model of myocardial ischemia was established. After drug treatment of 15 d， an electrocardiogram （ECG） was performed to analyze the degree of myocardial injury. A fully automatic biochemical analyzer was used to detect the changes in the serum levels of total cholesterol （TC）， high-density lipoprotein cholesterol （HDL-C）， triglyceride （TG）， and low-density lipoprotein cholesterol （LDL-C）. Hematoxylin-eosin （HE） staining and Masson staining were used to observe myocardial histopathological changes. TdT-mediated dUTP nick end labeling （TUNEL） staining was used to detect cardiomyocyte apoptosis. Western blot was adopted to detect the protein levels of extracellular signal-regulated kinase 1/2 （ERK1/2）， phospho-ERK1/2 （p-ERK1/2）， p38 mitogen-activated protein kinase （p38 MAPK）， phospho-p38 MAPK （p-p38 MAPK）， B-cell lymphoma-2 （Bcl-2）-associated X （Bax）， Bcl-2， and cleaved cysteine aspartate proteolytic enzyme （cleaved Caspase-3）. ResultCompared with the control group， the ECG S-T segment decreased in the model group. The serum levels of TC， TG， and LDL-C were increased significantly （P<0.05）. The arrangement of myocardial tissue was disordered， and the proportion of cardiomyocyte apoptosis increased. The protein levels of cleaved Caspase-3， Bax， and p-p38 MAPK in the heart were increased， and the Bcl-2 expression was decreased （P<0.05）. Compared with the model group， the S-T segment downward shift was restored in the low and high-dose Guipitang groups and trimetazidine group， and the levels of TC， TG， and LDL-C were decreased. The protein expression of cleaved Caspase-3 and Bax in the heart dropped， and p-p38 MAPK and p-ERK1/2 protein expressions increased significantly （P<0.05）. The degree of myocardial injury was alleviated， and the proportion of cardiomyocyte apoptosis decreased. Bcl-2 protein expression was increased significantly in the low-dose Guipitang group （P<0.05）. ERK1/2 and p38 MAPK proteins had no significant difference among different groups. ConclusionGuipitang could alleviate myocardial injury and inhibit cardiomyocyte apoptosis in rats by activating the expression of ERK1/2 and p38 MAPK.
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Objective:To investigate the influence of T2DM Spleen-qi Deficiency syndrome on Ankle-Brachial Index (ABI).Methods:The clinical data of 298 patients with T2DM who were hospitalized in Dongzhimen Hospital, Beijing University of Chinese Medicine from January 2019 to December 2021 were retrospectively analyzed. According to the diagnostic criteria of spleen-qi deficiency syndrome, the patients were divided into two groups: spleen-qi deficiency syndrome group and non-spleen-qi deficiency syndrome group. There were 142 patients in the spleen-qi deficiency syndrome group and 156 patients in the non-spleen-qi deficiency syndrome group. The differences of ABI between the two groups were compared, and the correlation between spleen-qi deficiency syndrome and clinical indicators (gender, age, body mass index, course of diabetes, history of hypertension, smoking history, fasting glucose, total cholesterol, triglyceride, platelet, hemoglobin, serum albumin, blood urea nitrogen, serum creatinine, estimated glomerular filtration rate) and ABI in T2DM patients was analyzed.Results:The left ABI [1.09 (1.00, 1.19) vs. 1.13 (1.03, 1.22)] and the right ABI [1.09 (0.96, 1.17) vs. 1.12 (1.02, 1.20)] in T2DM spleen-qi deficiency syndrome group were significantly lower than those in non-spleen-qi deficiency group ( P<0.05).The left ABI was significantly correlated with spleen-qi deficiency syndrome ( r=0.122, P=0.035) and estimated glomerular filtration rate ( r=0.137, P=0.018), and the right ABI was significantly correlated with spleen-qi deficiency syndrome ( r=0.123, P=0.034) and PLT ( r=-0.115, P=0.047). After correcting for other confounding factors by multiple linear regression analysis, there was significantly correlation between spleen-qi deficiency syndrome and ABI. Conclusion:Compared with the non-spleen-qi deficiency syndrome group, T2DM patients in the spleen-qi deficiency group had a lower ankle-brachial index and were more likely to develop peripheral arterial disease.
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AIM:To study the effect of roscovitine on the inflammatory hyperplasia of carotid artery intima in rats and the related mechanisms .METHODS: SD rats ( n=60 ) were randomly divided into 3 groups including control group, model group and treatment group .The rat model was established by trypsin digestion injury .The rats in control group were given sham operation .The rats in treatment group were administered with 0.5 mL roscovitine (2 g/L) slow-re-leasing gelatin.The rats in each group were fed normally for 4 weeks, then killed to take out carotid arteries for further ob-servations .The effects of roscovitine on the inflammatory hyperplasia of carotid artery intima and the related mechanism via nuclear factor-κB ( NF-κB) in the rats were detected by Western blot .RESUITS:Roscovitine inhibited the activation of NF-κB and the expression of inflammatory factors cyclooxygenase-2 (COX-2), vascular cell adhesion molecule-1 (VCAM-1),TNF-αand IL-6 via blocking the phosphorylation activation of NF-κB and inhibiting the degradation of IκB-α.CON-CLUSION:Roscovitine inhibits inflammatory hyperplasia of carotid artery intima in the rats via suppressing NF-κB activa-tion.