[Effects of liraglutide on the expression of local renin-angiotensin system, transforming growth factor-β1 and collagen type III in pulmonary tissue of diabetic rats].
Wei Zhao, Guangmin Chen, Bei Sun, Xiao Zheng, Qi Wu, Hong Zhang
Abstract
Wei Zhao, Guangmin Chen, Bei Sun, Xiao Zheng, Qi Wu, Hong Zhang
Abstract
OBJECTIVE: To explore the effects of GLP-1 receptor analog liraglutide on the expression of local renin-angiotensin system (RAS), TGF-β1 and collagen type III in pulmonary tissue of diabetic rats. METHODS: Thirty male Wistar rats were divided into normal (N), diabetic (DM) and liraglutide treatment (LR) groups according to the table of random number. Diabetes mellitus was induced by feeding with a high-sugar and high-fat diet and a low-dose injection of streptozotocin into caudal vein for 8 weeks. After successful modeling, liraglutide (400 µg×kg(-1)×d(-1)) was administered by a subcutaneous injection for 12 weeks in LR group. At Week 12, the mRNA expression levels of AT1R and TGF-β1 were detected by real-time quantitative polymerase chain reaction (RT-qPCR), the protein expression of AngII was detected by enzyme-linked immunosorbent assay (ELISA) and the protein expression levels of AT1R and transforming growth factor-beta 1 (TGF-β1) were detected by Western blotting (WB). Collagen type III was detected by immunohistochemistry. RESULTS: The expressions of AT1R,AngII, TGF-β1 and collagen type III increased in DM group than those of N group (P < 0.05). The expressions of AT1R, AngII, TGF-β1 and collagen type III were lower in LR group than those of DM group (RT-qPCR of AT1R: 0.08 ± 0.04 vs 0.32 ± 0.16, WB of AT1R: 1.20 ± 0.11 vs 1.32 ± 0.05; ELISA of AngII: (2.78 ± 0.56) vs (4.04 ± 0.13) ng/L; RT-qPCR of TGF-β1: 0.21 ± 0.11 vs 0.64 ± 0.16, WB of TGF-β1:1.01 ± 0.15 vs 1.19 ± 0.13; mean optical density of Col III:0.11 ± 0.04 vs 0.27 ± 0.04, positive area ratio of Col III:0.056 ± 0.023 vs 0.090 ± 0.026, all P < 0.05). CONCLUSIONS: Liraglutide plays a role of organ protection by inhibiting the expression of TGF-β1 of pulmonary tissue of diabetic rats. And it may be related with a down-regulation of local RAS.
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OBJECTIVE: To explore the effects of GLP-1 receptor analog liraglutide on the expression of local renin-angiotensin system (RAS), TGF-β1 and collagen type III in pulmonary tissue of diabetic rats. METHODS: Thirty male Wistar rats were divided into normal (N), diabetic (DM) and liraglutide treatment (LR) groups according to the table of random number. Diabetes mellitus was induced by feeding with a high-sugar and high-fat diet and a low-dose injection of streptozotocin into caudal vein for 8 weeks. After successful modeling, liraglutide (400 µg×kg(-1)×d(-1)) was administered by a subcutaneous injection for 12 weeks in LR group. At Week 12, the mRNA expression levels of AT1R and TGF-β1 were detected by real-time quantitative polymerase chain reaction (RT-qPCR), the protein expression of AngII was detected by enzyme-linked immunosorbent assay (ELISA) and the protein expression levels of AT1R and transforming growth factor-beta 1 (TGF-β1) were detected by Western blotting (WB). Collagen type III was detected by immunohistochemistry. RESULTS: The expressions of AT1R,AngII, TGF-β1 and collagen type III increased in DM group than those of N group (P < 0.05). The expressions of AT1R, AngII, TGF-β1 and collagen type III were lower in LR group than those of DM group (RT-qPCR of AT1R: 0.08 ± 0.04 vs 0.32 ± 0.16, WB of AT1R: 1.20 ± 0.11 vs 1.32 ± 0.05; ELISA of AngII: (2.78 ± 0.56) vs (4.04 ± 0.13) ng/L; RT-qPCR of TGF-β1: 0.21 ± 0.11 vs 0.64 ± 0.16, WB of TGF-β1:1.01 ± 0.15 vs 1.19 ± 0.13; mean optical density of Col III:0.11 ± 0.04 vs 0.27 ± 0.04, positive area ratio of Col III:0.056 ± 0.023 vs 0.090 ± 0.026, all P < 0.05). CONCLUSIONS: Liraglutide plays a role of organ protection by inhibiting the expression of TGF-β1 of pulmonary tissue of diabetic rats. And it may be related with a down-regulation of local RAS.
Key concepts: Liraglutide, Internal medicine, Endocrinology, Renin–angiotensin system, Transforming growth factor, Streptozotocin, Receptor, Angiotensin II