Inhibition of advanced glycation end-product formation on eye lens protein by rutin

Abstract

Formation of advanced glycation end products (AGE) plays a key role in the several pathophysiologies associated with ageing and diabetes, such as arthritis, atherosclerosis, chronic renal insufficiency, Alzheimer's disease, nephropathy, neuropathy and cataract. This raises the possibility of inhibition of AGE formation as one of the approaches to prevent or arrest the progression of diabetic complications. Previously, we have reported that some common dietary sources such as fruits, vegetables, herbs and spices have the potential to inhibit AGE formation. Flavonoids are abundantly found in fruits, vegetables, herbs and spices, and rutin is one of the commonly found dietary flavonols. In the present study, we have demonstrated the antiglycating potential and mechanism of action of rutin using goat eye lens proteins as model proteins. Under in vitro conditions, rutin inhibited glycation as assessed by SDS-PAGE, AGE-fluorescence, boronate affinity chromatography and immunodetection of specific AGE. Further, we provided insight into the mechanism of inhibition of protein glycation that rutin not only scavenges free-radicals directly but also chelates the metal ions by forming complexes with them and thereby partly inhibiting post-Amadori formation. These findings indicate the potential of rutin to prevent and/or inhibit protein glycation and the prospects for controlling AGE-mediated diabetic pathological conditions in vivo.

Glucose‐mediated protein glycation: Contribution of methanolic extract of Ceratonia siliqua L. in protection and in vitro potential inhibition of acetylcholinesterase

“…From these data, we can say that rutin is likely the main PC responsible of the antiglycation power of CsME and AChE inhibition ability. In fact, a multitude studies suggested that rutin presented antiglycation power (Cervantes-Laurean et al, 2006;Muthenna, Akileshwari, Saraswat, & Bhanuprakash Reddy, 2012;Nagasawa et al, 2003), inhibited α-glucosidase (Li, Zhou, Gao, Bian, & Shan, 2009), and exhibited antidiabetic action (Suan Chua, 2013). Moreover, a study (Richetti et al, 2011) reported the neuroprotective effect of rutin against scopolamine-induced memory impairment in zebrafish.…”

A detailed image of rutin underlying intracellular signaling pathways in human SW480 colorectal cancer cells based on miRNAs‐lncRNAs‐mRNAs‐TFs interactions

“…On the contrary, rutin derivatives markedly inhibit AGEs formation (Muthenna, Akileshwari, Saraswat, & Reddy, 2012), modify the extracellular matrix structure, and prevent the abnormal protein accumulation (Kamalakkannan & Prince, 2006).…”

Etiology and Prevention of Cataract

“…In the case of secondary cataract like diabetic cataract, the protein breakdown process is accelerated during hyperglycemia. Aldose reductase facilitates the transfer of glucose into sorbitol, which is impermeable to the membrane; accumulation of sorbitol ends with glycative and osmotic stress [ 89 ]. Any injury pertaining in the lens tissue may lead to hydration of the protein causing dense cortical cataract.…”

“…Aldose reductase facilitates the conversion of glucose to sorbitol using NADPH as the cofactor. Accumulation of sorbitol results in osmotic swelling, osmotic gradient, and tissue damage [ 89 ]. The patho-mechanism is convicted by the formation of advanced glycation end products, the end products of millard reaction culminates in lens protein alteration.…”