| مستخلص: |
Objective: To investigate effects of adiponectin on survival, oxidative stress, inflammation and mitochondrial function of endothelial cell HUVEC induced by high glucose, and its potential mechanism. Methods: HUVEC cells were cultured with 5, 25 mmol/L glucose and divided into normal (NC) group and high glucose (HG) group. Adiponectin (1, 2, 4 µg/ml) treatment of high glucose induced endothelial cells were divided into low dose (L), medium dose (M) and high dose (H) groups. HUVEC cells treated with PBS, LPS and 4 µg/ml adiponectin were labeled as H+PBS group and H+LPS group. CCK8 and Annexin V-FITC/PI double staining were used to detect cell proliferation and apoptosis. Western blot was used to detect protein expressions of Cleaved caspase-3, NLPR3, amino acid transporter (ASC), Caspase-1, p-nuclear factor κB inhibitor protein (p-I-κBα) . ELISA was used to detect concentrations of lactate dehydrogenase (LDH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), malondialdehyde (MDA), IL-4, IL-6 and IL-1β. ROS fluorescence activity was detected by immunofluorescence. Mitochondrial membrane potential was detected by JC-1 staining. NLRP3 expression was detected by RT-qPCR. Results: Compared with NC group, 48 h, 72 h and 96 h survival rates of endothelial cells were significantly reduced, apoptosis rate was significantly increased, and levels of LDH, SOD, MDA, mitochondrial membrane potential, IL-4, IL-6 and IL-1β in cell supernatant were significantly increased, concentrations of ROS and GSH-Px were significantly decreased, and protein expressions of Cleared caspase-3, NLRP3, Caspase-1 and p-NF-κB were significantly increased, p-I-κBα expression was decreased significantly (P<0.05) . Adiponectin inhibited above changes of endothelial cells induced by high glucose in a concentration dependent manner. LPS attenuated above protective effects of adiponectin on HG induced endothelial cells. Conclusion: Adiponectin can reduce survival inhibition, oxidative stress, inflammatory response and mitochondrial dysfunction of endothelial cells induced by high glucose, whose protecting mechanism may be related to NF-κB pathway. [ABSTRACT FROM AUTHOR] |
