DIHYDROMYRICETIN ATTENUATES HIGH GLUCOSE-INDUCED CASPASE 3 EXPRESSION, ROS PRODUCTION AND INCREASES AMPK PHOSPHONYLATION IN PC12 CELLS

Shumei Wang,Haijian Li,Bao Li,Chunzhen Zhao,Lin Wang,Shuo Wang,Zhenzhen Li

doi:10.32553/jbpr.v8i5.674

Shumei Wang, Haijian Li + Show 5 more

Open Access

https://doi.org/10.32553/jbpr.v8i5.674

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Abstract

Dihydromyricetin (DMY) has a protective effect on neural function under central nervous system dysfunction conditions. There is growing interest concerning the beneficial effects of DMY on treating diabetic neuropathy (DN). This study was carried to detect protective effects of DMY on high glucose (HG)-induced cell damage and related mechanisms. The effect of DMY on cell survival was detected by MTT assay. Caspase-3 and phosphorylated AMP-activated protein kinase (AMPK) was evaluated by Western blotting. The effects of DMY and AMPK agonist AICAR on ROS production was determined. Our results showed that DMY treatment protect against HG-induced cell damage. DMY treatment significantly reduced the expression of caspase-3 and phosphorylated AMPK. ROS production was inhibited by DMY or AMPK agonist AICAR treatment. These studies demonstrate that DMY may inhibit ROS production, caspase-3 expression through AMPK pathway. Keywords: dihydromyricetin, caspase, oxidative stress

Highlights

IntroductionDiabetic neuropathy (DN) is one of the most common diabetes-related complications leading to cognitive impairment, motor and sensory dysfunction[1]
Diabetes mellitus is a major cause of high morbidity and mortality in the world
Many evidence have reported that overproduction of reactive oxygen species (ROS) contributed to neural cell apoptosis and inhibition of oxidation may block the progression of Diabetic neuropathy (DN)[3]

Summary

Introduction

Diabetic neuropathy (DN) is one of the most common diabetes-related complications leading to cognitive impairment, motor and sensory dysfunction[1]. Oxidative stress, impaired cerebral insulin signaling systems are considered as being closely related to DN development[2]. Many evidence have reported that overproduction of reactive oxygen species (ROS) contributed to neural cell apoptosis and inhibition of oxidation may block the progression of DN[3]. Dihydromyricetin (DMY), a flavonoid compound, was isolated from the leaves of Ampelopsis grossedentata[4]. It has been reported to possess multiple pharmacological activities including antiinflammatory[5], anti-oxidative[6], anticancer[7] and hepatoprotective effects[8]. Recent data supported dihydromyricetin attenuated methylglyoxal induced- oxidative stress in PC12 cells[9]

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