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Effect of melatonin on expression of α-SMA and E-cadherin in mice with bleomycin-induced pulmonary fibrosis |
HU Qingqing, ZHOU Enmin, Jin Ke, DU Yong, QIAN Yan, WENG Huachun |
Department of Pediatrics, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325015 |
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Cite this article: |
HU Qingqing,ZHOU Enmin,Jin Ke, et al. Effect of melatonin on expression of α-SMA and E-cadherin in mice with bleomycin-induced pulmonary fibrosis[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2018, 48(8): 577-581.
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Abstract Objective: To investigate the effect of melatonin on expression of α-SMA and E-cadherin in mice with bleomycin induced pulmonary fibrosis and its mechanism. Methods: Mice pulmonary fibrosis model was made by intratracheal injection of bleomycin (5.0 mg/kg) and randomly divided as model group and melatonin group. After 4 weeks, the mice were sacrificed and lung tissue extracted. HE staining was used to evaluate the morphological changes and the oxidative stress kit was used to detect the activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA). The levels of inflammatory cytokines IL-6 and TNF-α in lung tissues were measured by RT-PCR. The expression of α-SMA and E-cadherin in lung tissue was detected by immunohistochemistry. The expression of α-SMA and E-cadherin mRNA in lung tissue was detected by RT-PCR. Western blot was used to detect the expression of α-SMA and E-cadherin in lung tissue. Results: Compared with the model group, the SOD expression in the melatonin group was significantly increased (P<0.05), and the MDA expression was significantly decreased (P<0.05); the expression of TNF-α and IL-6 in the lung tissue was significantly decreased (P<0.05). Immunohistochemistry results showed that the expression of α-SMA protein in the lung tissue of melatonin group was significantly reduced (P<0.05), and E-cadherin protein expression was significantly increased (P<0.05); RT-PCR experiment results showed that the expression of α-SMA mRNA in the lungs of melatonin mice was significantly decreased (P<0.05), and E-cadherin mRNA expression was significantly increased (P<0.05). Western blot results showed that the expression of α-SMA protein in lung tissue of melatonin mice was significantly decreased (P<0.05), and E-cadherin protein expression was significantly increased (P<0.05). Conclusion: Melatonin can inhibit the expression of α-SMA protein, reduce the expression of E-cadherin, and delay the progression of pulmonary fibrosis by reducing the levels of oxidative stress and inflammatory factors.
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