Objective To study the expression of cyclooxygenase-2 (COX-2) in the gastric epithelial carcinogensis and its relation with cell apoptosis and proliferation. Methods 15 cases of normal gastric mucosa (NGM), 30 cases of intestinal metaplasia (IM), 30 cases of dysplasia (Dys) and 40 cases of gastric cancer (GC) were used in this study. The expressions of COX-2 and proliferating cell nuclear antigen (PCNA) were detected by immunohistochemical SABC method, and cell apoptosis was measured by TUNEL. Results The expression level of COX-2 gradually increased from NGM, IM, Dys to GC. The positive rate of COX-2 in GC was 67.5%, 13.3% in NGM, and 33.3% in IM. There was a significant difference in COX-2 expression between GC and IM, GC and NGM(P0.05). The expression of COX-2 in poorly differentiated cancer was markedly higher than that in well differentiated cancer (P

Objective:To observe the effect of diammonium glycyrrhizinate injection on bronchus,lung tissue and amount of eosinophils(EOS)in rats with asthma and to discuss the mechanism of diammonium glycyrrhizinate intervention on airway inflammation in asthma.Methods:To divide 60 male SD rats into 6 groups as following:normal control group,model group,dexameth group,high dose of diammonium glycyrrhizinate group,middle dose of diammonium glycyrrhizinate group and low dose of diammonium glycyrrhizinate group(n=10).After setting up the model of rats with asthma,we detect the EOS in both rats'blood serum and bronchoalveolar lavage and observe the pathological change in bronchus and lung tissue in rats of each group.Results:Not only the amount of EOS of rats in model group is bigger than that in normal control group(P

[Objective]To investigate the protective effect of Zhuangtongyin on the Middle Cerebral Artery Occlusion(MCAO)model by modulating ferroptosis through the Nrf2-SCL7A11/xCT-Gpx4 pathway and its underlying mechanism.[Methods]C57BL/6J mice were randomly divided into Sham operation group(Sham),model group(MCAO),low-dose Zhuangtongyin group(ZTY-L),high-dose Zhuangtongyin group(ZTY-H),with 5 mice in each group.The MCAO group was modelled by silica gel embolization,the middle cerebral artery of mice was embolized for 1h,then the silica gel was pulled out and reperfusion was performed after 72 h;and the other operations in the Sham group were the same as those in the MCAO group except that the thread plug was not inserted.The neural function of mice was evaluated by Zea-Longa method.TTC staining was used to evaluate the volume of cerebral infarction.The level of brain injury was evaluated by HE staining and Nissl staining.Prussian blue staining and the expression of iron transport-related carrier receptors TfR1 and DMT1 on mRNA level was detected by qPCR to evaluate the iron ion deposition level in mice brain.The expression of lipid peroxidation-related gene ACSL4 on mRNA level was detected by qPCR,and the content of 4-HNE was detected by ELISA kit to evaluate the lipid peroxidation level of mice brain.The expressions of ferroptosis marker PTGS2 mRNA level was detected by qPCR.The expressions of Nrf2,SCL7A11/xCT,Gpx4 in mice brain tissue were detected by Western-blot and immunofluorescence.[Results]Zhuangtongyin improved the nerve function of mice after MCAO(P＜0.05)and the cerebral infarction volume of mice(P＜0.05)and alleviate the pathological injury of cerebral cortex cells after MCAO operation.Zhuangtongyin attenuated the accumulation of trivalent iron ions in the brain tissue of mice following MCAO.Additionally,Zhuangtongyin downregulated the expression of TfR1 and DMT1 mRNA(P＜0.001),a transporter associated with cellular iron ion uptake,in the brains of post-MCAO mice.Furthermore,Zhuangtongyin reduced levels of lipid peroxidation product 4-HNE(P＜0.001)and suppressed ACSL4 mRNA expression in brain tissue post-MCAO(P＜0.001).Besides,Zhuangtongyin downregulated the expression of PTGS2 mRNA(P＜0.001),in the brains of post-MCAO mice.Zhuangtongyin increased the expression of nrf2 into the nucleus(P＜0.001),and increased the expression of xCT and Gpx4 in neurons after MCAO(P＜0.001).[Conclusion]Zhuangtongyin can enhance the nerve function and reduce cerebral infarction volume in MCAO/R mice,alleviate the pathological damage of cerebral cortex cells,and modulate the expression of key signaling molecules in the Nrf2-SCL7A11/xCT-Gpx4 pathway.Therefore,it is suggested that the mechanism by which Zhuangtongyin improves MCAO/R injury in mice may involve regulating ferroptosis through the Nrf2-SCL7A11/xCT-GPX4 pathway.