Pyrroloquinoline quinone alleviates oxidative damage induced by high glucose in HepG2 cells

被引:7
|
作者
Alkahtani, Saad [1 ]
Alarifi, Saud [1 ]
Alkahtane, Abdullah A. [1 ]
Albasher, Gadah [1 ]
AL-Zharani, Mohammed [2 ]
Alhoshani, Norah M. [1 ]
AL-Johani, Norah S. [1 ]
Aljarba, Nada H. [3 ]
Hasnain, Md Saquib [4 ]
机构
[1] King Saud Univ, Coll Sci, Dept Zool, POB 2455, Riyadh 11451, Saudi Arabia
[2] Imam Muhammad Ibn Saud Islamic Univ, Coll Sci, Dept Biol, Riyadh, Saudi Arabia
[3] Princess Nourah bint Abdulrahman Univ, Coll Sci, Dept Biol, Riyadh, Saudi Arabia
[4] Palamau Inst Pharm, Dept Pharm, Daltonganj 822102, Jharkhand, India
关键词
Pyrroloquinoline quinone; Glucose; Oxidative stress; Cancer; GLYCATION END-PRODUCTS; OXYGEN RADICALS; STRESS; HYPERGLYCEMIA; N-EPSILON-(CARBOXYMETHYL)LYSINE; COMPLICATIONS; ANTIOXIDANT; PROTECTS; EXTRACT; LIVER;
D O I
10.1016/j.sjbs.2021.06.063
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Hyperglycemia as a common metabolic disorder in diabetes led to oxidative stress, inflammation and other complications. Natural and manufactured antioxidants alleviates the side effects of diabetes. The purpose of current study is to investigate the effect of pyrroloquinoline quinine (PQQ) as an antioxidant on the content of glucose-induced oxidative stress generation in the cells of the human hepatocellular liver carcinoma (HepG2) by inhibiting advanced glycation end products (AGEs) formation. The HepG2 cells were exposed to high dose (50 mM) of glucose (HG) only and with PQQ (HG + PQQ). Treatment with high dose increased AGEs formation, expression of receptor for advanced glycation endproducts (RAGE), reactive oxygen species ROS production, and oxidative stress markers in treated HepG2 cells. Interestingly, PQQ significantly reduced AGEs formation and (RAGE) expression, ROS formation, and inflammation induced by glucose. In conclusion, PQQ has a potentiail role as an antioxidant to reduce the oxidative damage during hyperglycemia by AGEs inhibition. (C) 2021 The Author(s). Published by Elsevier B.V. on behalf of King Saud University.
引用
收藏
页码:6127 / 6132
页数:6
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