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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.
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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.
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Objective To observe the interfering effect of different doses of penehyclidine hydrochloride (PHC) on the mRNA expressions of nuclear factor kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) in the lung tissue of rats with traumatic shock so as to investigate the protective role of PHC in secondary long injury following traumatic shock and the underlying mechanism.Methods The traumatic shock model was established.A total of 104 Wistar rats were randomly divided into four groups:control group,shock group,low dose PHC group ( P1 group) and high dose PHC group ( P2 group).At the beginning of resuscitation,the rats in P1 and P2 groups were given transjugular intravenous injection of 2 ml/kg isotonic saline containing 0.15 mg/kg and 0- 45 mg/kg PHC respectively,while the rats in shock and control groups were injected only isometric isotonic saline.The rats in the four groups were killed at 2 h,6 h,12 h and 24 h after resuscitation respectively to detect the mRNA expressions of NF-κB and iNOS by using RT-PCR and determine the lung wet/dry weight (W/D) ratio,lung permeability index (LPI) and lung injury score (LIS).Results The mRNA expressions of NF-κB and iNOS,lung W/D ratio,LPI and LIS at all the time intervals in the shock,P1 and P2 groups were all significantly increased as compared with those in the control group (P＜0.05).Howerver,the P2 group showed significant reduction in aspects of the mRNA expressions of NF- κB and iNOS,lung W/D ratio,LPI and LIS at all time points and P1 group also had significant decrease regarding the mRNA expressions of NF-κB and iNOS,lung W/D ratio at2 h,6 h,and LPI and LIS at 2 h,6 h,12 h,as compared with the shock group.Meanwhile,P2 group showed evident decrease at 6 h concerning the mRNA expressions of NF-κB and iNOS,lung W/D ratio,LPI and LIS as compared with P1 group (P ＜ 0.05 ).Conclusions PHC,especially at a large dosage,can significantly mitigate the long injury secondary to traumatic shock,and the mechanism may be associated with the inhibition of mRNA expressions of NF-κB and iNOS.