Effect of Coenzyme Q10 on nutrient sensor gene expression in AKI animal model following Hemiscorpius lepturus envenomation

Acute kidney injury (AKI) is correlated to imbalance in mitochondrial homeostasis and coenzyme Q10 (CoQ10) content. Decline in CoQ10 as one of the main electron carriers can cause decreased in adenosine triphosphate (ATP). It supposed that AMPK, Sirtuin1 and 3 as a key metabolism regulator in nutritional stress condition, stimulate energy production via mitochondrial biogenesis in AKI condition. Although much is known about energy sensing pathways, the precise role of CoQ10 level and nutrient sensor gene expression in envenomation induced AKI remains to be obscure.Our data showed significant decrease in CoQ10 level after 5 and 10 mg/kg envenomation. Besides, a significant over expression of Sirt1observed in 5 and 10 mg/kg after 24 h of treatment and only 5 mg/kg after one week compared with control groups. While, over expression of Sirt3 and AMPK observed in 5 mg/kg after 24 h and one week treatment compare to control animals(P<0.05). Also, significant increase in caspase-9 and 3gene expression after 5 and 10 mg/kg of envenomation confirmed involvement of cell death signaling.Overall, reduced in CoQ10 level as the main antioxidant and intermediate in energetics pathway increases the overexpression of Sirt3, Sirt1 and MAPK which plays a key role in energy homeostasis in recovery stage of AKI following envenomation.

کلیدواژه ها:

Venom induced AKI ، CoQ10 ، Sirt1 ، Sirt3 ، and AMPK