ScopeReusing deep‐fried oil is a common practice to cut costs, and their consumption may affect brain function. Hence, the study investigates the modulatory potential of Lactobacillus fermentum MCC2760 (LF) on heated oil‐induced brain oxidative stress (OS) and inflammation that may have a bearing on cognition in experimental rats.Methods and resultsFemale Wistar rats are fed with diets containing native sunflower oil (N‐SFO), native canola oil (N‐CNO), heated sunflower oil (H‐SFO), heated canola oil (H‐CNO), heated sunflower oil with probiotic (H‐SFO + LF), or heated canola oil with probiotic (H‐CNO + LF} for 60 days. Compared to respective controls, heated oils significantly (p < 0.05) increased OS by decreasing antioxidant defense enzymes and nuclear factor erythroid 2‐related factor 2 (NRF2) activity. Further, heated oil elevates brain expression of cytosolic phospholipase A2 (cPLA2), cyclooxygenase‐2 (COX‐2), prostaglandin‐E receptor 4 (EP‐4), intercellular adhesion molecule 1 (ICAM‐1), nitric oxide synthase 2 (NOS‐2), followed by an increased production of proinflammatory eicosanoids (prostaglandin E2 [PGE2] and leukotriene B4 [LTB4]) and cytokines (tumor necrosis factor‐α [TNF‐α], monocyte chemoattractant protein‐1 [MCP‐1], interleukin‐1β [IL‐1β], and interleukin‐6 [IL‐6]). The increased nuclear translocation of nuclear factor kappa beta (NF‐kB) in heated oil‐fed groups’ brains corroborates the heightened inflammatory response. Heated oils decrease neurotrophins and neuron development markers. However, administration of LF abrogates the heated oil‐induced alterations significantly (p < 0.05).ConclusionsThe present study is novel in demonstrating the protective role of probiotic LF against heated‐oil‐induced brain OS and inflammation in rats.

中文翻译：

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发酵乳杆菌 MCC2760 通过调节大鼠的 NRF2 和 NF-kB 来减轻加热油诱导的脑氧化应激和炎症


范围重复使用油炸油是降低成本的常见做法，食用油炸油可能会影响大脑功能。因此，该研究调查了发酵乳杆菌 MCC2760 （LF） 对加热油诱导的脑氧化应激 （OS） 和炎症的调节潜力，这可能对实验大鼠的认知产生影响。方法和结果雌性 Wistar 大鼠饲喂含有天然葵花籽油 （N-SFO）、天然菜籽油 （N-CNO）、加热葵花籽油 （H-SFO）、加热菜籽油 （H-CNO）、加热葵花籽油与益生菌 （H-SFO + LF） 或加热菜籽油与益生菌 （H-CNO + LF}） 60 天。与各自的对照相比，加热油 （p < 0.05） 通过降低抗氧化防御酶和核因子红细胞 2 相关因子 2 （NRF2） 活性显着增加 OS。此外，加热的油会提高细胞溶质磷脂酶 A2 （cPLA2）、环氧合酶-2 （COX-2）、前列腺素-E 受体 4 （EP-4）、细胞间粘附分子 1 （ICAM-1）、一氧化氮合酶 2 （NOS-2） 的表达，随后促炎性类花生酸（前列腺素 E2 [PGE2] 和白三烯 B4 [LTB4]）和细胞因子（肿瘤坏死因子 α [TNF-α] 的产生增加， 单核细胞趋化蛋白-1 [MCP-1]、白细胞介素-1β [IL-1β] 和白细胞介素-6 [IL-6]。在加热的油喂养组的大脑中，核因子 kappa β （NF-kB） 的核易位增加证实了炎症反应的增强。加热的油会降低神经营养因子和神经元发育标志物。然而，LF 的施用显着消除了加热的油诱导的改变 （p < 0.05）。结论本研究在证明益生菌 LF 对热油诱导的大鼠脑 OS 和炎症的保护作用方面具有新颖性。