Therapeutic effect of naringenin on diabetes retinopathy rats by regulating JAK2/STAT3/SOCS1 signaling pathway
10.3760/cma.j.cn115807-20240408-00099
- VernacularTitle:柚皮素调节JAK2/STAT3/SOCS1信号通路对糖尿病视网膜病变大鼠的疗效研究
- Author:
Yanli SUN
1
;
Lifang ZHANG
;
Jian CHENG
Author Information
1. 宁波大学附属人民医院眼科中心，宁波 315000
- Keywords:
Naringenin;
Diabetes mellitus;
JAK2/STAT3/SOCS1 signaling pathway;
Diabetes retinopathy
- From:
Chinese Journal of Endocrine Surgery
2024;18(4):549-553
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the therapeutic effect of naringenin on diabetes retinopathy (DR) rats by regulating Janus kinase 2 (JAK2) /signal transducer and activator of transcription 3 (STAT3) /suppressor of cytokine signaling 1 (SOCS1) signaling pathway.Methods:A DR rat model was constructed and randomly separated into DR group, naringenin group, activator group, and naringenin+activator group, with normal rats as the control group. After intervention according to corresponding groups, blood glucose and glycosylated hemoglobin of rats were detected. Retinal tissue was separated, and interleukin-6 (IL-6), IL-1β, glutathione (GSH), and catalase (CAT) were detected. The pathological changes in rats and blood retinal vascular barrier permeability were detected, and the retinal tissue adhesion factor 1 (VCAM-1), anti vascular endothelial growth factor (VEGF) mRNA, and JAK2/STAT3/SOCS1 pathway related proteins were detected.Results:In the control group, blood glucose levels were (5.16±0.53) mmoL, glycosylated hemoglobin (4.26±0.45) %, IL-6 (63.11±6.35) pg/mL, IL-1β (23.11±2.38) pg/mL, Evans blue (EB) content (4.72±0.49) ng/mg, VCAM-1 (1.02±0.11), VEGF mRNA expression (0.93±0.10), p-JAK2/JAK2 (0.24±0.03), p-STAT3/STAT3 (0.19±0.02), GSH (17.62±1.81) nmoL/mg, CAT (11.68±1.19) IU/mg, and SOCS1 expression 1.44±0.16; while in DR group, blood glucose were (18.85±1.89) mmoL, HBA1c (11.62±1.18) %, IL-6 (89.17±8.99) pg/mL, IL-1β (52.11±5.28) pg/mL, EB (10.24±1.08) ng/mg, VCAM-1 1.56±0.16, VEGF 1.61±0.18, P-JAK2/JAK2 0.55±0.06 and P-STAT3/STAT3 0.47±0.05, all decreased compared with that of the control group ( P<0.05). The expressions of GSH were (8.27±0.88) nmoL/mg, CAT (6.85±0.71) IU/mg and SOCS1 0.86±0.09 in group DR, all increased compared with those of the control group ( P<0.05). In naringin group, blood glucose was (13.11±1.34) mmoL, HBA1c (7.36±0.76) %, IL-6 (67.08±6.75) pg/mL, IL-1β (31.61±3.22) pg/mL, EB content was (6.15±0.63) ng/mg, VCAM-1 1.15±0.12, VEGF mRNA expression 1.17±0.12, P-JAK2 /JAK2 0.29±0.03, and P-STAT3 /STAT3 0.21±0.03, all lower than those in DR Group ( P<0.05). However, the expressions of GSH were (15.22±1.59) nmoL/mg, CAT (10.95±1.11) IU/mg, and SOCS1 (1.37±0.15) ,all higher than those of DR group ( P<0.05). The activator reversed the protective effect of naringenin on DR Rats. Conclusion:Naringenin improves DR rat injury by regulating the JAK2/STAT3/SOCS1 signaling pathway.
