Protective effect of platycodin D on liver injury in alloxan-induced diabetic mice via regulation of Treg/Th17 balance |
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| Affiliation: | 1. State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China;2. Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, China;3. School of Pharmacy, China Pharmaceutical University, Nanjing 210009, China;4. Changchun University of Chinese Medicine, Changchun 130117, China;1. Department of Biomedical Science and Technology and M.A.T.I. Center of Excellence, University of Udine, Udine, Italy;2. Experimental Diabetes Unit, Division of Immunology, Transplantation and Infectious Diseases, San Raffaele Scientific Institute, Milan, Italy;3. Mediterranean Institute for Transplantation and Advanced Specialized Therapies, ISMETT, Palermo, Italy;4. Department of Human Pathology, University of Palermo, Palermo, Italy;1. State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China;2. College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China;3. State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China;1. Department of Pharmacology, Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai 200025, China;2. Department of Pharmacy, Shanghai Institute of Health Sciences and Health School Attached to SJTU-SM, 279 Zhouzhu Road, Shanghai 201318, China |
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| Abstract: | Platycodin D is a major pharmacological constituent of Platycodi Radix with immunomodulatory activity. The present study was designed to investigate how platycodin D (PLD) reveals liver injury in diabetic mice and its mechanism. Fifty mice were divided into five groups randomly: control group, model group, rosiglitazone (ROG, 10 mg/kg) group, PLD (50 mg/kg) group, and PLD (100 mg/kg) group. Diabetes was induced with the injection of alloxan monohydrate (150 mg/kg) subcutaneously, and animals with blood glucose level of ≥ 250 mg/dl were considered as diabetic mice. After the first day of diabetes induction, the treatments were performed for 8 weeks. Then the animals were anaesthetized, and blood and liver samples were also collected for further assay. PLD significantly decreased the serum levels of glucose, insulin, interleukin-6 (IL-6), interleukin-1β, tumor necrosis factor-α (TNF-α), and interleukin (IL)-17A and increased IL-10 level in serum. PLD effectively downregulated aspartate transaminase (AST), alanine aminotransferase (ALT), total cholesterol (TC), and triglycerides (TG) in liver. PLD also attenuated liver histological change. In addition, PLD significantly attenuated IL-17A and IL-10 levels in vitro, flow cytometry (FCM) studies also showed that PLD remarkably inhibited Th17 cells and significantly increased Treg cells in liver tissues and spleen cells. Western blot demonstrated PLD inhibited the phosphorylation of JAK and STAT-3 and the expression of RORγt and increased the expression of Foxp3. The findings showed that PLD exerts beneficial effects on alloxan-induced liver injury in mice. |
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