|
|
The effect of geniposide on mice with diabetic nephropathy |
CHEN Jundixia, PAN Xiaoqiong, YU Bowei, HU Zhen |
Department of Traditional Chinese Medicine, the Second Affiliated Hospital of Wenzhou Medical University, Wenzhou 325027, China |
|
Cite this article: |
CHEN Jundixia,PAN Xiaoqiong,YU Bowei, et al. The effect of geniposide on mice with diabetic nephropathy[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2019, 49(9): 644-648.
|
|
Abstract Objective: To investigate the effect of geniposide on diabetic nephropathy. Methods: Diabetic mice were established by streptozotocin and randomly divided as model group, geniposide low dose group (100 mg/kg), high dose group (200 mg/kg) and normal control group. The model group and the normal group were given normal saline, and the geniposide dose groups were given the corresponding dose intragastrically for 8 weeks. The living conditions of the mice were observed and recorded. The body weight and blood glucose were measured. The pathological changes of renal tissue were observed by HE staining, and the expression of TNF-α, IL-6 and IL-1β mRNA were detected by RT-qPCR. Results: Compared with the normal control group, the model group had poorer life quality, slower weight gain (P<0.01), increased blood glucose (P<0.01), and obviously damaged glomerular structure shown by pathological staining. A large number of interstitial inflammatory cells were infiltrated, and the expression of TNF-α, IL-6 and IL-1β in renal tissue was increased, as detected by RT-qPCR assay (P<0.01). Compared with the model group, the mice in the low and high dose groups had a better living conditions, more rapid increase of the body weight (P<0.05), significantly decreased blood glucose (P<0.01) but improved pathological morphology of renal tissue and decreased expression of TNF-α, IL-6 and IL-1β in renal tissue (P<0.01). Conclusion: Geniposide can improve the symptoms of diabetes in mice and protect the kidney tissues. Its regulatory mechanism may be related to the improvement of inflammation in diabetic mice.
|
Received: 26 April 2019
|
|
|
|
|
[1] GIUGLIANO D, CERIELLO A, ESPOSITO K. Glucose metabolism and hyperglycemia[J]. Am J Clin Nutr, 2008, 87(1): 217-222.
[2] BABAEI-BALDERLOU F, ZARE S, HEIDARI R, et al. Effects of melatonin and vitamin E on peripheral neuropathic pain in streptozotocin-induced diabetic rats[J]. Iran J Basic Med Sci, 2010, 13(2): 1-8.
[3] MAGEE C, GRIEVE D J, WATSON C J, et al. Diabetic nephropathy: a tangled web to unweave[J]. Cardiovasc Drugs Ther, 2017, 31(5-6): 579-592.
[4] MAUER S M, STEFFES M W, ELLIS E N, et al. Structural-functional relationships in diabetic nephropathy[J]. J Clin Invest, 1984, 74(4): 1143-1155.
[5] NAVARRO J F, MORA C. Role of inflammation in diabetic complications[J]. Nephrol Dial Transplant, 2005, 20(12): 2601-2604.
[6] NAVARRO-GONZÁLEZ J F, MORA-FERNÁNDEZ C. The role of inflammatory cytokines in diabetic nephropathy[J]. J Am Soc Nephrol, 2008, 19(3): 433-442.
[7] SHAN M, YU S, YAN H, et al. A review on the phytochemistry, pharmacology, pharmacokinetics and toxicology of geniposide, a natural product[J]. Molecules, 2017, 22(10): 1689-1718.
[8] KIM T H, YOON S J, LEE S M. Genipin attenuates sepsis by inhibiting Toll-like receptor signaling[J]. Mol Med, 2012, 18: 455-465.
[9] SHIN D, LEE S, HUANG Y H, et al. Protective properties of geniposide against UV-B-induced photooxidative stress in human dermal fibroblasts[J]. Pharm Biol, 2018, 56(1): 176-182.
[10] ZHANG Y, DING Y, ZHONG X, et al. Geniposide acutely stimulates insulin secretion in pancreatic β-cells by regulating GLP-1 receptor/cAMP signaling and ion channels[J]. Mol Cell Endocrinol, 2016, 430: 89-96.
[11] ZHAO C, ZHANG H, LI H, et al. Geniposide ameliorates cognitive deficits by attenuating the cholinergic defect and amyloidosis in middle-aged Alzheimer model mice[J]. Neuropharmacology, 2017, 116: 18-29.
[12] WANG L, WU G, WU F, et al. Geniposide attenuates ANIT-induced cholestasis through regulation of transporters and enzymes involved in bile acids homeostasis in rats[J]. J Ethnopharmacol, 2017, 196: 178-185.
[13] WANG J, CHEN L, LIANG Z, et al. Genipin inhibits LPS-induced inflammatory response in BV2 microglial cells[J]. Neurochem Res, 2017, 42(10): 2769-2776.
[14] SHI Q, CAO J, FANG L, et al. Geniposide suppresses LPS-induced nitric oxide, PGE2 and inflammatory cytokine by downregulating NF-κB, MAPK and AP-1 signaling pathways in macrophages[J]. Int Immunopharmacol, 2014, 20(2): 298-306.
[15] ZHENG H, WHITMAN S A, WU W, et al. Therapeutic potential of Nrf2 activators in streptozotocin-induced diabetic nephropathy[J]. Diabetes, 2011, 60(11): 3055-3066.
[16] 姚冬冬, 舒娈, 杨蕾, 等. 栀子苷降糖作用及相关机制研究[J]. 中草药, 2014, 45(8): 1121-1125.
[17] NAVARRO-GONZÁLEZ J F, MORA-FERNÁNDEZ C, MUROS DE FUENTES M, et al. Inflammatory molecules and pathways in the pathogenesis of diabetic nephropathy[J]. Nat Rev Nephrol, 2011, 7(6): 327-340.
[18] HATANAKA E, MONTEAGUDO P T, MARROCOS M S, et al. Neutrophils and monocytes as potentially important sources of proinflammatory cytokines in diabetes[J]. Clin Exp Immunol, 2006, 146(3): 443-447.
[19] SAHAKYAN K, KLEIN B E, LEE K E, et al. Inflammatory and endothelial dysfunction markers and proteinuria in persons with type 1 diabetes mellitus[J]. Eur J Endocrinol, 2010, 162(6): 1101-1105. |
|
|
|