Anand Santosh, Azam Ansari Mohammad, Kumaraswamy Sukrutha Sambamurthy, Alomary Mohammad N, Anwar Khan Anmar, Elderdery Abozer Y
Department of Biotechnology, School of Applied Sciences, REVA University, Bengaluru, Karnataka, India.
Department of Epidemic Disease Research, Institutes for Research and Medical Consultations, Imam Abdulrahman Bin Faisal University, Dammam 31441, Saudi Arabia.
Neuroscience. 2022 Dec 15;507:139-148. doi: 10.1016/j.neuroscience.2022.11.001. Epub 2022 Nov 11.
Inflammation and resolution are highly programmed processes involving a plethora of immune cells. Lipid mediators synthesized from arachidonic acid metabolism play a pivotal role in orchestrating the signaling cascades in the game of inflammation. The majority of the studies carried out so far on inflammation were aimed at inhibiting the generation of inflammatory molecules, whereas recent research has shifted more towards understanding the resolution of inflammation. Owing to chronic inflammation as evident in neuropathophysiology, the resolution of inflammation together with the class of lipid mediators actively involved in its regulation has attracted the attention of the scientific community as therapeutic targets. Both omega-three polyunsaturated fatty acids, eicosapentaenoic acid and docosahexaenoic acid, orchestrate a vital regulatory role in inflammation development. Resolvins derived from these fatty acids comprise the D-and E-series resolvins. A growing body of evidence using in vitro and in vivo models has revealed the pro-resolving and anti-inflammatory potential of resolvins. This systematic review sheds light on the synthesis, specialized receptors, and resolution of inflammation mediated by resolvins in Alzheimer's and Parkinson's disease.
炎症和炎症消退是高度程序化的过程,涉及大量免疫细胞。由花生四烯酸代谢合成的脂质介质在炎症过程中协调信号级联反应中起关键作用。迄今为止,大多数关于炎症的研究旨在抑制炎症分子的产生,而最近的研究更多地转向了解炎症的消退。由于神经病理生理学中明显存在的慢性炎症,炎症的消退以及积极参与其调节的脂质介质类别作为治疗靶点已引起科学界的关注。ω-3多不饱和脂肪酸二十碳五烯酸和二十二碳六烯酸在炎症发展中都起着至关重要的调节作用。源自这些脂肪酸的消退素包括D系列和E系列消退素。越来越多使用体外和体内模型的证据揭示了消退素的促消退和抗炎潜力。本系统综述阐明了消退素在阿尔茨海默病和帕金森病中介导的炎症的合成、特异性受体和消退情况。