Evaluating the effect of hydro-alcoholic extract of Phoenix dactylifera L. spathe on streptozotocin-induced diabetic rats

Hosseinzadeh, Azam; Jani, Ali; Karimi, Mahdi; Siahpoosh, Amir; Goudarzi, Mehdi; Malayeri, Alireza

doi:10.1007/s00580-021-03221-4

Cited by 1 publication

(1 citation statement)

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“…This metabolic disorder occurs when the pancreas is unable to generate sufficient amounts of insulin or when the cells of target tissues fail to respond to insulin. 1 Hyperglycemia induces oxidative stress and activates various signaling pathways leading to the development of different diabetic complications including micro-(nephropathy, neuropathy and retinopathy) and macro-vascular (ischemic heart disease, peripheral vascular disease, and cerebrovascular disease) complications 2,3 ; these complications are the main causes of mortality and morbidity in diabetic patients with poor blood glucose control. 4 In tissues, glucose is autoxidized to form a-dicarbonyl compounds such as glyoxal (GO) and methylglyoxal (MG).…”

Section: Introductionmentioning

confidence: 99%

Lovastatin attenuates glyoxal-induced toxicity on rat liver mitochondria

et al. 2021

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Alpha-dicarbonyls such as glyoxal (GO) trigger mitochondrial dysfunction resulting in the development of different diabetic complications. The present study investigated the effects of lovastatin against GO-induced toxicity on rat liver mitochondria. The rat liver mitochondria (0.5 mg protein/mL) were treated with various concentrations of lovastatin (1, 5, 10 µM) at 37°C for 30 min and then exposed to GO (3 mM) at 37°C for 30 min. Oxidative stress markers including MDA, reactive oxygen species (ROS), glutathione (GSH) and protein carbonylation (PC) level were measured. Mitochondrial complex II activity and mitochondrial membrane potential (MMP) were assessed for evaluating mitochondrial function. Glyoxal significantly increased the level of ROS, PC and MDA. This effect was associated with the reduction of MMP, complex II activity and GSH content. Pre-treatment with lovastatin potentially reversed GO-induced mitochondrial toxicity. These results suggest that lovastatin have a protective effect against GO-induced toxicity in isolated rat liver mitochondria.

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Section: Introductionmentioning

confidence: 99%