ABSTRACT
<p><b>OBJECTIVE</b>To study on the effect and mechanism of curcumin on inhibiting injury induced by free radical in pulmonary fibrosis.</p><p><b>METHOD</b>One hundred and forty-four male SD rats were randomly divided into 6 groups (24 rats in each group). Rats in the model control group, positive medicine group, and high, moderate and low curcumin groups were injected with a single dose of bleomycin by trachea, and rats in sham-model control group with same volume normal saline. One day after the injection, curcumin solution of different dosages (200,100,50 mg x kg(-1) x d(-1)) was respectively given to rats in the high, moderate and low curcumin group by daily gastrogavage, while equal volume of normal saline was given to those in the sham-model control group and model control group, and an equal volume of prednisone (0.56 mg x kg(-1) x d(-1)) was saline was given to those in positive medicine control group. On the 7, 14, 28 days, the contents of GSH-Px, SOD, MDA and iNOS in pulmonary tissues of different groups were measured.</p><p><b>RESULT</b>Curcumin can raise the content of SOD and GSH-Px and lessen the level of MDA and iNOS.</p><p><b>CONCLUSION</b>Curcumin can regulate the level of free radical in the body of rats with pulmonary fibrosis and lessen the oxidative injury of pulmonary tissues caused by free radical, in the body of rats with pulmonary fibrosis. The mechanisms of curcumin on idiopathic pulmonary fibrosis lie in adjusting the level of free radical and inhibiting the injury of lung tissue induced by free radical.</p>
Subject(s)
Animals , Male , Rats , Antioxidants , Pharmacology , Bleomycin , Curcuma , Chemistry , Curcumin , Pharmacology , Free Radicals , Metabolism , Glutathione Peroxidase , Metabolism , Lung , Metabolism , Pathology , Malondialdehyde , Metabolism , Nitric Oxide Synthase Type II , Metabolism , Plants, Medicinal , Chemistry , Pulmonary Fibrosis , Metabolism , Random Allocation , Rats, Sprague-Dawley , Superoxide Dismutase , MetabolismABSTRACT
Objective To observe the expression of bcl-2 gene in cell apoptosis of neonatal rats followed by hypoxic-ischemic brain damage(HIBD) and investigate the mechanism of neuronal apoptosis after HIBD.Methods Fifty-four neonatal SD rats were used in 1 sham-operated group and 8 trial groups. The models of HIBD were established in neonatal rats by inhaling the mixed gases of 92 % N 2 and 8 % O 2, the animals were sacrificed by dislocation their heads at different time points(0.5,1,3,6,12,24,48,72 h), the hippocampus were dissected for morphological analysis. The neuronal apoptosis and the expression of bcl-2 gene in hippocampus were detected by the methods of immunohistochemistry. Results The apoptotic cells appeared at the time point of 3 h, and reached the peak at 48 h, then decreased. The positive cell of bcl-2 protein increased from the time point of 30 min and reached the peak at 6 h and then decreased gradually following HIBD. Conclusion The expression of bcl-2 gene plays a role in the process of neuronal apoptosis following HIBD.