Publications (2)0 Total impact
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ABSTRACT: To observe the expression of p-p38 mitogen-activated protein kinase in lung tissues of acute lung injury rat model induced by lipopolysaccharide (LPS) and to explore the protective effects of melatonin (MT) in lung tissues in rats. Seventy-two rats was randomly assigned to three groups, control group, LPS group and LPS + MT group. Rat model of ALI was established by instilling LPS intratracheally. We used immunohistochemical SP and Western blot method to detect the expression of p-p38 mitogen-activated protein kinase in lung tissues and used light microscope to observe morphological changes. There were rare p-p38 mitogen-activated protein kinase positive cells scattered in alveolar and airway epithelial cells in control group (P < 0.01). The positive p-p38 mitogen-activated protein kinase cells in LPS group increased obviously than those in control group (P < 0.01), and were mainly distributed in infiltrative inflammatory cells, airway epithelial cells, alveolar epithelial cells and pleurames epithelial cells. In MT group, the p-p38 mitogen-activated protein kinase positive cells in airway and lung tissues were much less than those in the LPS group (P < 0.05). The Western blot results were consistent with those of immunohistochemical method. The expression of p-p38 mitogen-activated protein kinase increases in alveolar and airway epithelial cells in acute lung injury rat models induced by LPS. The activation of p-p38 mitogen-activated protein kinase is found in most lung tissues, suggesting that p-p38 mitogen-activated protein kinase participates in the signal transduction in inflammatory and noninflammatory cells. MT is an effective antioxidant, which relieves the inflammation in acute lung injury rats, possibly through the inhibition of the pathway of p38 MAPK over activation.Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology 11/2010; 26(4):481-4.
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ABSTRACT: To investigate the protective effect of melatonin (MT) on lung tissues during acute lung injury (ALI) in rats and its possible mechanism. Seventy-two Sprague-Dawley (SD) rats were randomly divided into three groups: control group, lipopolysaccharide (LPS) group and MT treatment group. In LPS group and MT treatment group, 1 ml/kg of LPS (200 mug/200 mul) was administered through the airway. In MT group, 10 mg/kg of MT was injected intraperitoneally before and after administration of LPS, and 1 ml/kg of ethanol-normal saline was given in control rats. The rats were sacrificed at 3, 6, 10 hours after administration of LPS, and the lung tissue was obtained for determination of the contents of nitrogen monoxide (NO) and malondialdehyde (MDA), and activity of superoxide dismutase (SOD). In addition, the expression of phosphorylation p38 mitogen-activated protein kinase (p-p38 MAPK) in lung tissue was assayed with immunohistochemistry staining. Compared with control group, SOD activity (U/mg) decreased significantly in LPS group (3 hours: 73.78+/-3.62 vs. 112.69+/-3.26, 6 hours : 66.07+/-2.31 vs. 117.85+/-1.96, 10 hours: 55.13+/-5.26 vs. 118.27+/-2.16, all P<0.01), but NO (micromol/mg), MDA (nmol/mg) content and the expression of p-p38 MAPK [absorbance (A) value] increased obviously (NO: 8.19+/-0.48 vs. 2.32+/-0.20 at 3 hours, 11.71+/-0.27 vs. 2.08+/-0.15 at 6 hours, 16.53+/-0.60 vs. 2.76+/-0.21 at 10 hours; MDA: 11.43+/-0.68 vs. 2.86+/-0.21 at 3 hours, 19.63+/-1.29 vs. 2.85+/-0.19 at 6 hours, 26.63+/-2.00 vs. 2.84+/-0.28 at 10 hours; p-p38 MAPK: 0.340+/-0.020 vs. 0.238+/-0.019 at 3 hours, 0.410+/-0.016 vs. 0.218+/-0.024 at 6 hours, 0.578+/-0.066 vs. 0.238+/-0.036 at 10 hours, all P<0.01). The administration of MT mitigated above contents significantly [SOD (U/mg) was 86.02+/-2.81, 80.87+/-3.40, 94.46+/-5.03, NO (micromol/mg) was 3.80+/-0.28, 5.32+/-0.22, 7.24+/-0.52, MDA (nmol/mg) was 8.18+/-0.84, 7.84+/-0.78, 6.43+/-1.06, and p-p38 MAPK (A value) was 0.311+/-0.018, 0.312+/-0.019, 0.314+/-0.021 at 3, 6, 10 hours, respectively, P<0.05 or P<0.01]. MT possessed protective effect on lung tissues during ALI by its antioxidation effect and inhibition of over- expression of p-p38 MAPK.Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue 07/2010; 22(7):418-21.
Hebei Medical University
Chentow, Hebei, China
- School of Basic Medical Sciences