Effect of Quamoclit angulata Extract Supplementation on Oxidative Stress and Inflammation on Hyperglycemia-Induced Renal Damage in Type 2 Diabetic Mice.
Ji Eun ParkHeaji LeeHyunkyung RhoSeong Min HongSun Yeou KimYunsook LimPublished in: Antioxidants (Basel, Switzerland) (2020)
Type 2 diabetes mellitus (T2DM) is caused by abnormalities of controlling blood glucose and insulin homeostasis. Especially, hyperglycemia causes hyper-inflammation through activation of NLRP3 inflammasome, which can lead to cell apoptosis, hypertrophy, and fibrosis. Quamoclit angulata (QA), one of the annual winders, has been shown ameliorative effects on diabetes. The current study investigated whether the QA extract (QAE) attenuated hyperglycemia-induced renal inflammation related to NLRP inflammasome and oxidative stress in high fat diet (HFD)-induced diabetic mice. After T2DM was induced, the mice were treated with QAE (5 or 10 mg/kg/day) by gavage for 12 weeks. The QAE supplementation reduced homeostasis model assessment insulin resistance (HOMA-IR), kidney malfunction, and glomerular hypertrophy in T2DM. Moreover, the QAE treatment significantly attenuated renal NLRP3 inflammasome dependent hyper-inflammation and consequential renal damage caused by oxidative stress, apoptosis, and fibrosis in T2DM. Furthermore, QAE normalized aberrant energy metabolism (downregulation of p-AMPK, sirtuin (SIRT)-1, and PPARγ-coactivator α (PGC-1 α)) in T2DM mice. Taken together, the results suggested that QAE as a natural product has ameliorative effects on renal damage by regulation of oxidative stress and inflammation in T2DM.
Keyphrases
- oxidative stress
- diabetic rats
- nlrp inflammasome
- glycemic control
- high fat diet
- insulin resistance
- blood glucose
- ischemia reperfusion injury
- induced apoptosis
- dna damage
- type diabetes
- high glucose
- skeletal muscle
- metabolic syndrome
- heat shock
- blood pressure
- cell proliferation
- cardiovascular disease
- endothelial cells
- cell death
- preterm birth
- fatty acid
- high speed