ABSTRACT
Objective To investigate the effects of cholinergic pathway on acute renal tubular cell injury induced by acute oxygen and glucose deprivation. Methods Rat kidney macrophages were isolated and cultured for constructing macrophages and renal epithelial cells co-cultivating model of oxygen-glucose deprivation (OGD), and the model cells were divided into three groups: OGD alone group, acetylcholine (ACh 100μmol/L)+OGD group and ACh + galantamine (Gal 10μmol/L)+OGD group. The cells underwent OGD treatment for 1 hour, and normally cultured for 24 hours. The expressions of TNF alpha, IL-1 beta, and IL-10 in supernatant fluid were detected by ELISA, the renal tubular cell viability was determined by MTT assay, the expression of acetylcholine esterase (AChE) mRNA and protein were determined by RT-qPCR and Western blotting. The activity of AChE was determined by colorimetric method. Results The expressions of TNF alpha (pg/ml) in OGD, Ach+OGD group, Ach+Gal+OGD groups were 140.2±44.81, 119.46±4.42 and 103.31±1.62 respectively (P0.05); The values of renal tubular cell proliferation were 55.02%±6.28%, 66.65%±6.47%, and 79.75%±4.22% respectively (P0.05); those of AchE protein were 0.66±0.07, 0.74±0.04 and 0.67±0.06 respectively (P>0.05); The activity of AChE (kU/L) was 0.51±0.02, 0.35±0.05 and 0.32±0.04 respectively (P=0.001, 0.001 and 0.368). Conclusions ACh and Gal could inhibit the secretion of inflammatory mediators and cholinesterase activity and can reduce the acute hypoxic renal tubular cell injury. The modulation of the cholinergic pathway in macrophages may be the important treatment method for acute renal injury in the future.
ABSTRACT
Objective To study the protection effect of dexmedetomidine and ulinastatin on acute lung in-jury caused by hepatic ischemia reperfusion. Methods 50 rats were randomly divided into 5 groups: the blank group, saline group, the dexmedetomidine group, the ulinastatin group, the dexmedetomidine and ulinastatin group. Ischemia-reperfusion models were established and drugs were administrated through femoral vein. The levels of MDA, SOD and ICAM were detected. Results Compared with the blank group, the rest of the groups of PaO2, pH and SOD activity were significantly lower (P < 0.05), and BE, pathological grading, MDA, ICAM levels were significantly higher (P<0.05). PaO2, pH and SOD activity of ulinastatin group were significantly lower in the phys-iological saline group (P < 0.05), BE, pathological grading, MDA level, ICAM levels were significantly elevated in the physiological saline group (P<0.05). Conclusion Combination of dexmedetomidine and ulinastatin have protection effect on acute lung injury caused by hepatic ischemia reperfusion, its mechanism may be related to in-hibit neutrophil aggregation, improve their antioxidant capacity and inhibition of lipid peroxidation.