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Peroxisomal Acyl-CoA Oxidase Type 1: Anti-Inflammatory and Anti-Aging Properties with a Special Emphasis on Studies with LPS and Argan Oil as a Model Transposable to Aging

机译:过氧化物酰亚胺酰基-CoA氧化酶1:抗炎和抗衰老性能,特别强调LPS和奥根油作为转移到老化的模型

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摘要

To clarify appropriateness of current claims for health and wellness virtues of argan oil, studies were conducted in inflammatory states. LPS induces inflammation with reduction of PGC1-α signaling and energy metabolism. Argan oil protected the liver against LPS toxicity and interestingly enough preservation of peroxisomal acyl-CoA oxidase type 1 (ACOX1) activity against depression by LPS. This model of LPS-driven toxicity circumvented by argan oil along with a key anti-inflammatory role attributed to ACOX1 has been here transposed to model aging. This view is consistent with known physiological role of ACOX1 in yielding precursors of specialized proresolving mediators (SPM) and with characteristics of aging and related disorders including reduced PGC1-α function and improvement by strategies rising ACOX1 (via hormonal gut FGF19 and nordihydroguaiaretic acid in metabolic syndrome and diabetes conditions) and SPM (neurodegenerative disorders, atherosclerosis, and stroke). Delay of aging to resolve inflammation results from altered production of SPM, SPM improving most aging disorders. The strategic metabolic place of ACOX1, upstream of SPM biosynthesis, along with ability of ACOX1 preservation/induction and SPM to improve aging-related disorders and known association of aging with drop in ACOX1 and SPM, all converge to conclude that ACOX1 represents a previously unsuspected and currently emerging antiaging protein.
机译:为了澄清当前促进奥根石油的健康和健康美德的适当性,在炎症状态下进行研究。 LPS将炎症诱导降低PGC1-α信号传导和能量代谢。摩尔根油保护肝脏免受LPS毒性的影响,并有趣地保存过氧化合物酰基-CoA氧化酶1型(ACOX1)抑制LPS的抑郁症。这种LPS驱动的毒性模型由奥根油避难,以及归因于ACOX1的关键抗炎作用,已经转移到模型老化。这种观点与ACOX1的已知生理作用一致,在专门的预晶体介质(SPM)的前体以及老化和相关疾病的特征,包括降低的PGC1-α功能和通过策略上升的ACOX1(通过荷尔蒙肠道FGF19和代谢中的Nordihydoguaieteratic酸的改进综合征和糖尿病条件)和SPM(神经变性疾病,动脉粥样硬化和中风)。延迟衰老以解决炎症导致SPM的改变,SPM改善大多数老龄化障碍。 ACOX1的战略代谢地点,SPM生物合成的上游,以及ACOX1保存/诱导和SPM的能力,以改善与ACOX1和SPM下降的衰老相关疾病和已知的老化结合,所有融合都会得出结论,即ACOX1代表先前未经证实的和目前出现的抗衰蛋白。

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