Hawthorn fruit acid consumption attenuates hyperlipidemia-associated oxidative damage in rats

Abstract

ContextHyperlipidemia is a highly prevalent risk factor for atherosclerosis and stroke. The currently available medications used to treat Hyperlipidemia cannot improve its oxidative stress damage. Consumption of hawthorn can regulate blood sugar and blood lipids, and its rich fruit acid is a natural antioxidant that can improve oxidative stress damage.ObjectiveThe present research aimed to investigate the protective effect of hawthorn fruit acid (HFA) on hyperlipidemia and to determine its potential molecular mechanism.Materials and methodsSprague-Dawley rats were fed a high-fat diet (HFD) to induce hyperlipidemia and treated orally with hawthorn fruit acids (HFA). Serum and liver levels of total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), superoxide dismutase (SOD), hydrogen peroxide (CAT), and malondialdehyde (MDA) were measured. Human hepatocellular carcinoma cell lines (HepG2) cells were treated with 0.1 mM oleic acid and HFA (0.125, 0.25 mg/mL), and intracellular TC, TG, HDL-C, SOD, CAT and MDA were measured. Changes in LDLR, HMGCR, Nrf2, HO-1, NQO1 protein and gene expression were analyzed by Western blot and qPCR.ResultsThis study found that HFA treatment effectively reduced the level of triglyceride, cholesterol, and glucose, and attenuated hepatic steatosis in rats. Additionally, oxidative stress damage of rats was effectively reduced by treatment with HFA. Western blot and qPCR analysis indicated that HFA treatment inhibited fat accumulation in HepG2 cells by upregulating LDLR and downregulating HMGCR gene expression. HFA inhibits oleic acid (OA)-induced oxidative damage to HepG2 by activating the Nrf2/HO-1 signaling pathway.ConclusionHFA administration can provide health benefits by counteracting the effects of hyperlipidemia caused by an HFD in the body, and the underlying mechanism of this event is closely related to the activation of the Nrf2/HO-1 signaling pathway.

Linear association of compound dietary antioxidant index with hyperlipidemia: a cross-sectional study

“…Wu et al ( 31 ) found that the substrates of G. frondosa decreased glutathione (GSH) and catalase activity, increased GSH peroxidase activity, inhibited oxidative stress, and increased bile acid synthesis to improve hypercholesterolemia. Feng et al ( 32 ) administered hawthorn fructofuranic acid (HFA) to rats. Found that activation of Nrf2/HO-1 signaling pathway could inhibit oleic acid (OA)-induced oxidative damage in a hepatocellular carcinoma cell line (HepG2), which in turn reduced oxidative stress damage in rats, effectively reduced triglyceride and cholesterol levels, attenuated hepatic steatosis and intervened in hyperlipidemia.…”

Metabolomics analysis reveals amelioration effects of yellowhorn tea extract on hyperlipidemia, inflammation, and oxidative stress in high-fat diet-fed mice

“…The excessive intake of high-fat diet (HFD) leads to an increase in plasma cholesterol levels, thereby posing a serious threat to cardiovascular health in humans (8). Studies have shown that chronic and excessive intake of HFD leads to adipose deposition in visceral organs (perirenal and epididymal adipose tissue), increasing chronic inflammation and leading to damage due to oxidative stress (9)(10)(11). Therefore, inhibition of chronic inflammation and oxidative stress damage could be an effective strategy to reduce the risk of metabolic diseases.…”

Metabolome combined with gut microbiome revealed the lipid-lowering mechanism of Xuezhiping capsule on hyperlipidemic hamster induced by high fat diet

“…The botanical drugs composed of XZP, including GP ( Dai et al, 2022 ; Rao et al, 2022 ), Hawthorn ( Peng et al, 2019 ; Feng et al, 2022 ) and FRR ( Song & Shen, 2021 ), have been extensively studied in regulating TC, TG, LDL-C, and HDL-C. Researches showed that GP extract increased AMPK activation and suppressed adipogenesis by decreasing the mRNA expression of encoding CCAAT/enhancer binding protein-α (C/EBPα), peroxisome proliferator-activated receptors γ (PPARγ), sterol regulatory element-binding protein 1c (SREBP1C), and fatty acid synthase (FAS) ( Park et al, 2014 ; Wang B. et al, 2020 ). In addition, GP extract elevated phosphatidylcholine metabolism decreased the level of trimethylamine N-oxide for antihyperlipidemia effect ( Wang et al, 2013 ).…”