Objective:To investigate the effects of lipopolysaccharide (LPS)on the acute lung injury (ALI)and expressions of aquaporin 1 (AQP1)and aquaporin 5 (AQP5)in lung tissue of the rats. Methods:Forty-eight SPF grade male Wistar rats were randomly divided into control group and LPS group (n=24).The rats in LPS group were intravenously injected with LPS to induce ALI models,and the rats in control group were injected with saline. The rats were sacrificed at 2,6,12 and 24 h,and the samples were collected after the successful modeling.The pathological changes of lung tissue were observed with HE staining;the lung wet/dry weight (W/D)ratio and lung permeability index were detected;ELISA was used to detect the levels of TNF-αand MIP-1α.The expression levels of AQP1 and AQP5 protein and mRNA were measured by Western blotting,immunohistochemistry and Real-Time PCR methods. Results:Compared with control group, the TNF-α and MIP-1α levels in LPS group were significantly elevated at 2,6 and 12 h (P<0.05),and at 24 h they were gradually reduced to the normal level. The HE staining results showed the alveolar and interstitial edema at 2 h after LPS injection,obviously in 12 h. The lung W/D ratios and pulmonary permeability indexes at different time points in LPS group were significantly higher than those in control group (P<0.05),and they reached the peak at 12 h.The expression levels of AQP1 and AQP5 mRNA and protein in lung tissue of the rats at different time points in LPS group were significantly lower than those in control group (P<0.01 ). Conclusion:LPS can induce ALI in the rats and down-regulate the expressions of AQP1 and AQP5;LPS is involved in the formation of pulmonary edema.

AIM: To investigate the changes of angiotensin II, its receptors and nitric oxide (NO) expression in rats with acute kidney injury (AKI) induced by endotoxin (LPS) and to assess the efficacy of different doses of dexamethasone (DXM). METHODS: Wistar rats were randomly divided into five groups as follows: control group (NC), LPS group, and DXM treatment groups of different doses of DXM (0.5, 1.0 and 5.0 mg/kg). The AKI group was injected with LPS through the lateral tail vein, and the intervention group was given different doses of DXM after LPS injection. Tissue samples were collected at 2, 6, 12 and 24 h after treatment. Serum creatinine and urea nitrogen levels were determined by automatic biochemical analyzer. H&E staining was used to observe renal histopathology. Serum TNF-α and MIP-1α levels were determined by ELISA. The expression of the angiotensin receptor 1 (AT1R) and angiotensin receptor 2 (AT2R) proteins were detected by Western blot and immunohistochemistry. Nitrate reductase was used to detect NO changes in the serum and renal tissues. RESULTS: The serum levels of serum TNF-α, MIP-1α, creatinine, and urea nitrogen were significantly increased in the LPS group compared with the control group (P<0.05). A similar trend was also observed in the levels of plasma and renal tissue AngII, renal tissue AT2R, serum and renal tissue NO (P<0.05). The expression of AT1R in renal tissue was significantly decreased in the LPS group compared with the control group (P<0.05). Pathological analysis showed that glomerular neutrophil infiltration and renal tubular epithelial cells swelling, vacuolar degeneration and necrosis in the LPS group. Prolongation LPS treatment resulted in more significant kidney damage. The serum levels of TNF-α, MIP-1α, creatinine, and urea nitrogen were significantly decreased in the DXM group compared with the LPS group (P<0.05). A similar trend was also observed in the levels of plasma and renal tissue AngII, renal tissue AT2R, serum and renal tissue NO in the DXM group (P<0.05). The expression of AT1R in renal tissue was significantly increased (P<0.05) in the DXM group compared with the LPS group, indicating the alleviation of kidney injury. Amongst these biomarkers, the levels of serum TNF-α, MIP-1α, plasma AngII showed the most significant decrease in the high dose DMX group (P<0.05). The levels of serum creatinine, urea nitrogen, kidney NO showed more significant decreases in the low and medium dose DMX groups (P<0.05). The levels of kidney AngII to dose and AT1R showed the most significant decrease in medium and high dose DXM groups (P<0.05). The levels of kidney AT2R and serum NO were not significantly different between the DXM treatment groups. CONCLUSION: LPS can induce AKI in rats that can be mitigated by DXM. The mechanism of DXM in protection against AKI may be related to the down-regulation of inflammatory factors such as AngII, AT2R, and NO, and the up-regulation of AT1R expression. Different doses of dexamethasone have different intervention effects for different effector molecules.

Objective:To investigate the expression and significance of the angiotensin Ⅱ and its receptors in lipopolysaccharide (LPS)-induced acute lung injury and acute kidney injury in rats.Methods:Forty eight Wistar rats were randomly divided into two groups: control group and endotoxin group (LPS group). LPS was injected through tail vein in LPS group, and the same amount of saline was injected through tail vein in control group.Samples were collected at 2 h, 6 h, 12 h and 24 h, respectively.The histopathology of lung and kidney was observed by HE staining.We detected lung wet/dry weight ratio, serum creatinine, urea nitrogen and Ang Ⅱ concentration in plasma, lung and kidney tissues by radioimmunoassay.Western blot and immunohistochemistry were used to detect the expression changes of AT1R and AT2R in lung and kidney tissue.Results:Compared with the control group, the pathology of lung and kidney tissue in LPS group showed different degrees of damage.The lung wet/dry weight ratio, serum creatinine and urea level in LPS group were significantly increased than that in control group( P<0.05). The Ang Ⅱ content in plasma increased significantly at 2 h and 6 h ( P<0.05), and the expression level of Ang Ⅱ in lung and kidney increased significantly at all time points ( P<0.05). The expression of AT1R in lung and kidney decreased significantly ( P<0.05), while the AT2R protein expression increased significantly ( P<0.05). Additionally the correlation analysis showed that the expression level of Ang Ⅱ and AT2R were positively correlated with lung and renal function, while the expression of AT1R was negatively correlated with lung and renal function. Conclusion:LPS results in the damage of lung and kidney function and the change of renin-angiotensin system.The changes of Ang Ⅱ and angiotension receptors were correlated with lung and kidney injury.Ang Ⅱ and angiotension receptors may be involved in LPS induced lung and kidney injury.