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Experimental Gerontology 2019-Nov

Hypolipidemic effect of pure total flavonoids from peel of Citrus (PTFC) on hamsters of hyperlipidemia and its potential mechanism.

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L'enllaç es desa al porta-retalls
Yun Ling
Zheng Shi
Xingliang Yang
Zhaowei Cai
Lixia Wang
Xuming Wu
Aiqin Ye
Jianping Jiang

Paraules clau

Resum

Citrus is a group of popular fruit that includes oranges, lemons, limes and grapefruit but research of its peel on hyperlipidemia and its mechanism is rare reported. We examined the effect of pure total flavonoids from peel of Citrus (PTFC), an extract from the peel of Citrus Changshan-huyou which is a popular fruit in China, on hamsters with hyperlipoidemia induced by high-fat diet (HFD). We found that PTFC significantly reduced levels of serum cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-c) and improved levels of alanine transaminase (ALT), aspartate transaminase (AST) and Alkaline phosphatase (ALP) which associated with liver function in golden hamsters. Liver pathological results confirmed that the liver pathological section of golden hamster treated with PTFC was significantly improved compared with that of HFD group. The content of main cholesterol metabolic enzymes Cholesterol 7a-hydroxylase (CYP7A1) in liver was obviously recovered with PTFC treatment. Further studies shown that PTFC attenuated oxidative stress and free radical damage through superoxide dismutase (SOD) and malonyldialdehyde (MDA) tests and inflammatory injury by levels of Tumor Necrosis Factor-alpha (TNF-α) and interleukin-6 (IL-6) both in serum and hepatocyte of golden hamsters. Moreover, PTFC increased levels of RNA and protein expression of Peroxisome proliferator-activated receptor-α (PPAR-α) and PPAR-γ in liver, fat and skeletal muscle of hyperlipidemia golden hamster, significantly. Our results suggested that PTFC could play a hypolipidemic role through improvement of liver function by antioxidant and anti-inflammatory effects in hyperlipoidemia hamsters, its mechanism of action may through activating of PPARα and PPARγ.

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