背景:芝麻油和葵花籽油是印度南部流行的食用油。油炸是一种常见的食物制备方法。高温油炸与几种疾病有关,包括癌症,糖尿病,和未知的代谢问题。没有关于油炸油对PUFA代谢和发病机理的影响的长期研究。因此,本研究旨在通过连续处理探讨油炸油对Wistar大鼠的影响。此外,研究了味精诱导Wistar大鼠神经毒性的病理生理学。
方法:本研究使用体重200-260g的Wistar大鼠。雌性大鼠分为五组(1)标准食物(对照组),(2)未加热的芝麻油(UHSO)以及标准食品,和(3)重新加热的芝麻油(RHSO)以及标准食物,(4)未加热的葵花籽油(UHSFO)以及标准食品,和(5)与标准食物一起再加热葵花籽油(RHSFO),并持续到F1代。此外,F1雄性大鼠用2g/kg体重的MSG处理10天,并处死主要组织。
结果:我们发现用RHSO和RHSFO治疗的大鼠显示体重增加。油炸油喂养的大鼠(RHSO和RHSFO)显示出总胆固醇的显着增加-100mg/dl,LDL-23mg/dl,&TAG-100mg/dl,与未加热的油鼠相比。肝功能测试显示,与未加热的油和对照组相比,RHSO和RHSFO中的AST和ALT水平显着升高。炎症标志物显示,与未加热的油和对照组相比,RHSO和RHSFO中的Hs-CRP(0.35mg/dl)和LDH水平(6000U/L)显着升高。RT-PCR结果显示,与UHSO和UHSFO组相比,抗氧化基因SOD(两倍)和GPX(3倍)显着升高。肝脏和结肠组织学显示RHSO和RHSFO处理的大鼠的细胞结构明显受损。Further,用未加热的油和MSG处理的大鼠显示出统计学上显著较高的神经可塑性基因CREB的mRNA表达,BDNF和降低的NMDA水平(UHSO,UHSFO)与再加热的油组(RHSO&RHSFO)相比。与对照组相比,RHSFO治疗的大鼠的促炎标志物TNF-α表达显着升高。与其他组相比,脑组织学显示用RHSO和RHSFO治疗的大鼠的神经胶质细胞变性中的局灶性损伤。
结论:本研究的结果证明,连续补充油炸再热油会增加血清TGL和氧化应激标志物。肝脏代谢受损和肠-肝-脑轴的参与增加了神经变性的风险。
BACKGROUND: Sesame oil and sunflower oil are popular cooking oils in southern India. Deep-frying is a frequent method of food preparation. Deep-frying at high temperatures has been linked with several disorders, including cancer, diabetes, and unknown metabolic problems. There have been no long-term investigations on the influence of deep-fried oils on PUFA metabolism and pathogenesis. As a result, the current study aimed to explore the effect of deep-fried frying oil on Wistar rats by continuous treatment. Furthermore, the pathophysiology of MSG-induced neurotoxicity in Wistar rats was investigated.
METHODS: Wistar rats weighing 200-260 g were used in this study. Female rats were divided into five groups fed with (1) standard chow (control group), (2) unheated sesame oil (UHSO) along with standard chow, and (3) reheated sesame oil (RHSO) along with standard chow, (4) unheated sunflower oil (UHSFO) along with standard chow, and (5) reheated sunflower oil (RHSFO) along with standard chow and continued up to F1 generation. Furthermore, F1 male rats were treated with MSG of 2 g/kg body weight for 10 alternative days and were sacrificed for major tissues.
RESULTS: We found that rats treated with RHSO and RHSFO showed increased body weight. Deep-fried oil-fed rats (RHSO and RHSFO) showed a significant increase in total cholesterol- 100 mg/dl, LDL- 23 mg/dl, & TAG-100 mg/dl, when compared to unheated oil rats. Liver function tests revealed that AST and ALT levels were significantly elevated in RHSO and RHSFO when compared to unheated oils and the control group. Inflammatory markers revealed that Hs-CRP (0.35 mg/dl) and LDH levels (6000 U/L) were significantly elevated in RHSO and RHSFO when compared to the unheated oils and control group. RT-PCR results showed significant elevation in the antioxidant genes SOD (twofold) and GPX (3-fold) when compared to UHSO and UHSFO groups. Liver and colon histology showed significant damage in the cell structure of RHSO and RHSFO-treated rats. Further, rats treated with unheated oils and MSG showed statistically significantly higher mRNA expression of neuroplasticity genes CREB, BDNF and reduced NMDA levels (UHSO, UHSFO) when compared to reheated oil groups (RHSO & RHSFO). Proinflammatory marker TNF-α expression was significantly elevated in RHSFO-treated rats when compared to control. Brain histology showed focal damage in glial cell degeneration in rats treated with RHSO and RHSFO when compared to other groups.
CONCLUSIONS: The results from the present study proved that continuous supplementation deep-fried reheated oil consumption increased serum TGL and oxidative stress markers. Impaired liver metabolism and the involvement of the gut-liver-brain axis increased the risk of neurodegeneration.