Protection of tauroursodeoxycholic acid on high glucose-induced human retinal microvascular endothelial cells dysfunction and streptozotocin-induced diabetic retinopathy rats
| Autor: | Jing Wang, Dong Qin, Xiaobin Jia, Juan Chen, Weiquan Bu, Jia-rui Yuan, Jun-Fei Gu, Gang Tian, Xuefeng Hou, Bing-jie Zhao, Li Zhang, Chao Li, Liang Feng, Zi-Bo Dong, Chun-fei Wang, Di Zhao, Nan Yang |
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| Rok vydání: | 2016 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Taurine medicine.medical_treatment Intraperitoneal injection Gene Expression Regulation Enzymologic Diabetes Mellitus Experimental Rats Sprague-Dawley Taurochenodeoxycholic Acid Mice 03 medical and health sciences chemistry.chemical_compound Western blot Internal medicine Drug Discovery medicine Animals Humans MTT assay Pharmacology Diabetic Retinopathy medicine.diagnostic_test Transcription Factor RelA Endothelial Cells Retinal Vessels Tauroursodeoxycholic acid Diabetic retinopathy Intercellular Adhesion Molecule-1 medicine.disease Streptozotocin Ursodeoxycholic acid Rats Glucose 030104 developmental biology Endocrinology chemistry Nitric Oxide Synthase medicine.drug |
| Zdroj: | Journal of Ethnopharmacology. 185:162-170 |
| ISSN: | 0378-8741 |
| DOI: | 10.1016/j.jep.2016.03.026 |
| Popis: | Ethnopharmacological relevance Tauroursodeoxycholic acid (TUDCA), one of the main ingredients from bear gall which hold “Clearing heat and detoxification, Removing liver fire for improving eyesight” functions, is formed by the conjugation of ursodeoxycholic acid (UDCA) with taurine. However, the limited information of TUDCA on protecting diabetic retinopathy (DR) has been known. The present study was conducted to evaluate the protection of TUDCA on high glucose-induced human retinal microvascular endothelial cells (HRMECs) dysfunction and streptozotocin (STZ)-induced diabetic retinopathy (DR) rats and the possible mechanism underlying was also explored. Materials and methods The proliferation of high glucose-induced HRMECs was determined by MTT assay. DR rats’ model was established by an administration of high-glucose-fat diet and an intraperitoneal injection of STZ (30 mg/kg). The cell supernatant and rats’ serum were collected for the assays of NO content by ELISA kits. Retinas were stained with hematoxylin and eosin (HE) to observe pathological changes. Immunohistochemical assay was applied to examine the protein expression of ICAM-1, NOS, NF-κB p65 and VEGF in rat retinas. Furthermore, western blot analysis was carried out to examine the protein expression of ICAM-1, NOS, NF-κB p65 and VEGF in high glucose-induced HRMECs. Results After treating with TUDCA, high glucose-induced HRMECs proliferation could be significantly inhibited. TUDCA (5.0 μM, 25.0 μM and 125.0 μM) could decrease NO content in high glucose-induced HRMECs. Furthermore, TUDCA (500 mg/kg/d and 250 mg/kg/d) also decrease NO content in serum of DR rats. Additionally, both immunocytochemistry analysis and western blot analysis showed that the over-expression of ICAM-1, NOS, NF-κB p65 and VEGF were significantly decreased by TUDCA. Conclusion The data indicated that TUDCA could ameliorate DR by decreasing NO content and down-regulating the protein expression of ICAM-1, NOS, NF-κB p65 and VEGF. Thus, our experimental results suggested that TUDCA might be a potential drug for the prevention and treatment of DR. |
| Databáze: | OpenAIRE |
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