Résumé
Ischemia and hypoxia cause functional damage to brain tissues during stroke， and when blood supply is restored to brain tissues after ischemia， a large number of free radicals and calcium overload cause cerebral ischemia-reperfusion injury， which further aggravates the condition. Autophagy is a self-protection mechanism that maintains the homeostasis of the intracellular environment， but excessive autophagy causes brain tissue damage. MiRNA is a small endogenous non-coding RNA molecule that regulate various physiological activities at the gene level by binding to complementary sequences in the 3 '- UTR of its target gene mRNA， leading to translation inhibition or mRNA degradation. MiRNA not only directly acts on autophagy related proteins， but also participates in autophagy regulation induced by ischemia/reperfusion through various signaling pathways. However， there is still a lack of systematic induction and analysis of miRNA regulation of autophagy signaling pathways induced by cerebral ischemia/reperfusion. This article reviews the regulation of cellular autophagy during cerebral ischemia/ reperfusion by miRNA-124， miRNA-298， miRNA-202-5p， miRNA-142， miRNA-26b and so on through different signaling pathways， providing a systematic and theoretical approach for the study of autophagy in stroke.
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<p><b>OBJECTIVE</b>To detect the expression of transient receptor potential canonical 1 (TRPC1) in a mouse model of ozone-induced lung inflammation and explore its role in lung inflammation.</p><p><b>METHODS</b>In a mouse model of lung inflammation established by ozone exposure, the expression of TRPC1 in the inflammatory lung tissues was detected by RT-PCR, Wstern blotting and immunohistochemistry.</p><p><b>RESULTS</b>Compared to the control mice, the mice exposed to ozone showed significantly increased expression level of TRPC1 mRNA and protein in the inflammatory lung tissues (P<0.05). Immunohistochemistry showed increased TRPC1 protein expressions in the alveolar epithelial cells, bronchial epithelial cells, and inflammatory cells in the inflammatory lung tissues (P<0.05). The mRNA and protein expression levels of TRPC1 were positively correlated with the counts of white blood cells, macrophages, neutrophils and lymphocytes in the bronchoalveolar lavage fluid of the exposed mice (P<0.01).</p><p><b>CONCLUSION</b>TRPC1 may play a role in ozone-induced lung inflammation in mice.</p>
Sujets)
Animaux , Souris , Liquide de lavage bronchoalvéolaire , Modèles animaux de maladie humaine , Expression des gènes , Inflammation , Anatomopathologie , Poumon , Métabolisme , Anatomopathologie , Ozone , Pneumopathie infectieuse , Métabolisme , Anatomopathologie , ARN messager , Canaux cationiques TRPC , MétabolismeRésumé
AIM: The study was undertaken to explore the dynamic changes of the concentration of nitric oxide(NO) in ischemic myocardium and its mechanism.METHODS: In vivo myocardial ischemia of mice and in vitro perfused isolated heart of rat were used in the experiment. The effects of severity and time of ischemia on NO production, NOS activity and mRNA were examined, respectively. RESULTS: There was a considerable difference (P
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AIM:To observe the effects of Sini decoction against pulmonary injury induced by ex vivo ischemia-reperfusion in rats. METHODS: The model of ischemia-reperfusion was established. Twenty-four Sprague-Dawley rats were randomly divided into Sham, I/R, and SND groups. Wet to dry lung weight ratio (W/D), mean pulmonary artery pressure (MPAP), SOD activity and MDA contents in pulmonary perfusate and tissue, NOS activity and NO contents in pulmonary tissue were detected. The pathologic changes in pulmonary tissue were also observed by light microscope. RESULTS: The morphological changes of pulmonary injury were alleviated in SND group. Wet/dry ratio, MPAP and MDA contents in pulmonary perfusate and tissue were significantly lower in SND group after ischemic/reperfusion. SOD activity in pulmonary perfusate and tissue, and NO contents in pulmonary tissue were significantly higher in SND group than those in I/R group. No significant difference in NOS activity in pulmonary tissue among three groups was observed. CONCLUSION: These results indicate that SND may have a protective effect on ischemia-reperfusion injured lung by its antioxidant activity and by adjusting NO level.