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OBJECTIVE: To probe into the effect of bisoprolol on H9C2 cardiomyocyte injury induced by ischemia reperfusion (I/ R) and its mechanism. METHODS: H9C2 cardiomyocytes were cultured in vitro and divided into the control group ( Control group ), hypoxia / reoxygenation ( H / R) model group ( Model group ), bisoprolol group (Bisoprolol group), bisoprolol + apoptosis signal-regulated kinase 1 (ASK1) recombinant protein group (Bisoprolol+ ASK1 group). Except for the Control group, the H9C2 cardiomyocytes were treated with H / R injury in the rest groups. The cell viability was detected by cell counting kit (CCK8) method; the cell apoptosis was detected by flow cytometry; the myocardial injury markers [ lactate dehydrogenase ( LDH ), cardiac troponin T ( cTnT )] and inflammatory factors [ interleukin 6 ( IL-6), interleukin 1β ( IL-1β) and tumor necrosis factor α (TNF-α)] levels were measured by enzyme-linked immunosorbent assay; the calcium ion concentration in cells was measured by laser confocal assay; the ASK1-c-Jun amino-terminal kinase ( JNK) / p38 mitogen-activated protein kinase ( p38 MAPK) signaling pathway-related protein expression was detected by Western blotting. RESULTS: Compared with the Control group, the H9C2 cell viability, LDH and cTnT levels were lower, the cell apoptosis rate, IL-6, IL-1β and TNF-α levels were higher, the calcium ion concentration, p-ASK1 / ASK1, p-JNK/ JNK and p-p38 MAPK/ p38 MAPK ratio were higher in the Model group, with statistically significant differences (P<0. 05). Compared with the Model group, the H9C2 cell viability, LDH and cTnT levels were higher, the cell apoptosis rate, IL-6, IL-1β and TNF-α levels were lower, the calcium ion concentration, p-ASK1 / ASK1, p-JNK/ JNK and p-p38 MAPK/ p38 MAPK ratio were lower in the Bisoprolol group and Bisoprolol + ASK1 group, with statistically significant differences ( P < 0. 05). Compared with the Bisoprolol group, the H9C2 cell viability, LDH and cTnT levels were lower, the cell apoptosis rate, IL-6, IL-1β and TNF-α levels were higher, the calcium ion concentration, p-ASK1 / ASK1, p-JNK/ JNK and p-p38 MAPK/ p38 MAPK ratio were higher in the Bisoprolol +ASK1 group, with statistically significant differences (P<0. 05). CONCLUSIONS: Bisoprolol can improve H9C2 cardiomyocyte injury induced by I/ R through inhibiting inflammatory response and calcium overload, its mechanism may related to the inhibition of ASK1-JNK/ p38 MAPK signaling pathway activation. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To observe the effects of kaempferol (KMP) on inflammatory response and cardiomyocyte apoptosis in rats with myocardial infarction (MI), and to explore its mechanism. METHODS: Fifty rats were randomly divided into the Sham operation group (Sham), model group (MI), KMP group (received KMP), DPQ group [received poly ADP-ribose polymerase-1 (PARP-1) inhibitor] and KMP + DPQ group [received KMP combined with PARP-1 inhibitor], with 10 rats in each group. Except for the Sham group, MI models were established by ligation of left anterior descending coronary artery in other groups. After the corresponding drug treatment, the cardiac function indexes of rats were examined by echocardiography, and the activities of serum creatine kinase isoenzyme (CK-MB), cardiac troponin I (cTnI) and tumor necrosis factor-α(TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) were detected by enzyme-linked immunosorbent assay, the pathological morphology of rat myocardium was observed by hemotoxylin and eosin staining, the apoptosis of rat cardiomyocytes was detected by TUNEL staining, and the levels of TNF-α, IL-6 and IL-1β protein and PARP-1 protein expression in myocardium was detected by Western blotting. RESULTS: Compared with MI group, left ventricular end-systolic diameter and left ventricular end-diastolic diameter in the KMP group and DPQ group decreased significantly, left ventricular fractional shortening, left ventricular ejection fraction and serum CK-MB and cTnI levels increased significantly, and the pathological damage of myocardial tissue was significantly alleviated, the apoptosis rate, the levels of inflammatory factors (TNF-α, IL-6 and IL-1β) decreased significantly, and the expression of inflammatory factor-related proteins and PARP-1 protein in myocardial tissue were significantly down-regulated, with statistically significant differences (P<0. 05). The improvement of cardiac function in the KMP+DPQ group was significantly better than that in the KMP group and DPQ group (P<0. 05). CONCLUSIONS: KMP may inhibit MI and cardiomyocyte apoptosis by down-regulating PARP-1 expression, thereby improving cardiac dysfunction in rats with MI. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To probe into the effects of renal artery embolization combined with Adrenal hydrazone tablets on coagulation function and renal function in patients with acute renal hemorrhage. METHODS: A total of 61 patients with acute renal hemorrhage admitted into the Ninth People’ s Hospital Affiliated to Shanghai Jiaotong University School of Medicine from Sept. 2019 to Sept. 2021 were selected and divided into the single treatment group ( n = 30) and the combined treatment group (n = 31) via random number table. The single treatment group was treated with renal artery embolization, while the combined treatment group received renal artery embolization combined with Adrenal hydrazone tablets. The renal function of two groups was compared. Plasma prothrombin time (PT), activated partial thrombin time ( APTT) and fibrinogen ( FIB) levels were determined by immunoturbidimetry, and tumor necrosis factor α (TNF-α), interleukin ( IL)-1 and IL-22 levels were determined by enzyme-linked immunosorbent assay. The treatment effects and incidence of complications were observed. RESULTS: After treatment, the levels of hematocrit and hemoglobin in the combined treatment group were higher than those in the single treatment group, and the heart rate was lower than that in the single treatment group, with statistically significant differences (P<0. 05). After treatment, the levels of serum creatinine, 24 h urine protein and blood urea nitrogen in the combined treatment group were lower than those in the single treatment group, the differences were statistically significant (P< 0. 05). After treatment, PT and APTT in the combined treatment group were longer than those in the single treatment group, and the levels of FIB, TNF-α, IL-1 and IL-22 were lower than those in the single treatment group, the differences were statistically significant ( P < 0. 05 ). The total effective rate in the combined treatment group was 96. 77% (30 / 31), higher than 76. 67% (23 / 30) in the single treatment group; the incidence of complications in the combined treatment group was 3. 23% (1 / 31), lower than 20. 00% (6 / 30) in the single treatment group, the difference was statistically significant ( P < 0. 05). CONCLUSIONS: Renal arterial embolization combined with Adrenal hydrazone tablets in the treatment of acute renal hemorrhage can improve the renal function and the coagulation function, effectively regulate the inflammatory reaction, with remarkable therapeutic effects. [ABSTRACT FROM AUTHOR]