To study the possible mechanism of the effect of glucagon-like peptide-1 (GLP-1) on injury to neonatal rat cardiomyocytes induced by hypoxia-reoxygenation. Lactate dehydrogenase activity [(210.0±11.5) vs (101.4±6.5) U/L] ,apoptosis rate [(8. 138±1. 512) vs(0. 575±0. 168)%] ,and caspase-3 activity [(44.52± 5.69)vs(19.98±1.97) ,all P<0.01] were all increased after hypoxia-reoxygenation. GLP-1 appears to directly act on cardiomyocytes and to protect them from hypoxia-reoxygenation injury [lactate dehydrogenase (190.2±9.0) U/ L, apoptosis rate (2.688±0.580) %, caspase-3 activity 30.34±4.18] mainly by inhibiting the apoptosis probably via the PBK/Akt signaling pathways.

Objective : To investigate the effect of chemotherapeutic drug resistance induced by CLDN18⁃ARH⁃GAP26 fusion mutation gene in gastric cancer cells , and to investigate the sensitization effect of ginsenoside in the treatment of chemotherapeutic drug resistance caused by the expression of CLDN18⁃ARHGAP26 fusion mutation gene. Methods : The side population (SP) cells and non⁃side population ( NSP) cells of gastric cancer cell line BGC⁃823 were labeled with immunomagnetic bead antibody , and the lentiviral vector with overexpression of CLDN18⁃ARHGAP26 fusion mutation gene was selected for transfection with NSP cells. qPCR was used to detect the mRNA levels of CLDN18⁃ARHGAP26 fusion mutation and ATP Binding Cassette Subfamily G Member 2 (ABCG2) . The expression of EMT⁃related proteins E ⁃Cadherin and Vimentin was detected by Western blot. The sensitivity of transfected cells to oxaliplatin was detected by CCK⁃8. The effect of ginsenoside on drug resistance of transfected cells was detected by CCK ⁃ 8 . The expression of E ⁃ Cadherin and Vimentin in transfected cells was detected by Western blot after ginsenoside treatment. Results : qPCR detection showed that the expression of CLDN18⁃ARH⁃GAP26 fusion mutant gene in NSP cells transfected with overexpressed CLDN18⁃ARHGAP26 fusion mutant gene was significantly higher than that of the non⁃transfected group , and the expression of ABCG2 mRNA was significantly cells with over⁃expressed CLDN18⁃ARHGAP26 fusion mutation gene was lower than that in the non⁃transfected transfected cells to oxaliplatin was lower than that in the non⁃transfected group. The survival rate of transfected cells sion of E ⁃Cadherin protein in the transfected cells treated with ginsenoside was higher than that in the untreated group , and the expression of Vimentin protein was lower than that in the untreated group. Conclusion Ginsenoside can reverse cell EMT transformation and oxaliplatin resistance induced by CLDN18⁃ARHGAP26 fusion mutated gene expression in gastric cancer tissues.