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Year : 2019  |  Volume : 15  |  Issue : 63  |  Page : 416-422

Pentamethylquercetin inhibited the growth of hepatic ascitic tumor cell H22 by improving metabolic environment and aerobic glycolysis in monosodium glutamate-induced obese mice

Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

Correspondence Address:
Wenqi Gao
Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pm.pm_605_18

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Aim: We investigated the effects of pentamethylquercetin (PMQ) on the tumor growth in monosodium glutamate (MSG)-induced obese mice. Materials and Methods: At the age of 5 weeks, control and MSG mice were, respectively, divided into five groups (n = 10): Vehicle group; PMQ 5, 10, 20 mg/kg; and metformin (MET) 300 mg/kg groups. All mice were administrated PMQ and MET by gastric gavage from 5- to 24-week age. 22-week-old mice were injection with H22 hepatic ascitic tumor cells. After 2 weeks, animals were anesthetized and blood, tumor, and liver tissues were harvested. Results: Compared with control mice, MSG mice showed obviously metabolic disorders and larger tumor weight and volume than those of control mice. PMQ and MET administration reduced body weight, improved glucose and lipid metabolism, and insulin resistance and inhibited tumor growth in MSG mice. However, PMQ and MET had a litter effect on the tumor growth and metabolic indexes in the control mice. Furthermore, there is significant positive correlation between improved insulin resistance and inhibited tumor growth by chronic PMQ and MET treatment. Further experiments showed PMQ and MET treatment upregulated mRNA expressions of sirtuin 6 (sirt6) both in tumor and liver tissues. Conclusion: Our results demonstrated PMQ decreased tumor growth in the MSG mice and the potential mechanisms might be attributed to upregulated mRNA expressions of sirt6.

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