title: 15d-PGJ2 Reduced Microglia Activation and Alleviated Neurological Deficit of Ischemic Reperfusion in Diabetic Rat Model.
abstract: To investigate the effect of PPARγ agonist 15d-PGJ2 treatment on the microglia activation and neurological deficit of ischemia reperfusion in diabetic rat model, adult Sprague-Dawley rats were sacrificed for the research. The rats were randomly categorized into four groups: (1) sham-operated group; (2) standard ischemia group; (3) diabetic ischemia group; (4) diabetic ischemia group with diabetes and treated with 15d-PGJ2. Compared to the sham-operated group, all the ischemic groups have significantly severer neurological deficits, more TNF-α and IL-1 expression, increased labeling of apoptotic cells, increased CD68 positive staining of brain lesion, and increased volume of infarct and cerebral edema in both 24 hours and 7 days after reperfusion. Interestingly, reduced neurological deficits, decreased TNF-α and IL-1 expression, less apoptotic cells and CD68 positive staining, and alleviated infarct and cerebral edema volume were observed when 15d-PGJ2 was intraperitoneally injected after reperfusion in diabetic ischemia group, suggesting its neuroprotective role in regulating microglia activation, which may have a therapeutic application in the future.
authors: Department of Neurology, Central Hospital of Zhabei District, Shanghai 200070, China.
authors: Lihong
authors: L
authors: Huang
authors: Department of Neurology, East Hospital, Medicine School of Tongji University, Shanghai 200120, China.
authors: Gang
authors: G
authors: Li
authors: Department of Neurology, Central Hospital of Zhabei District, Shanghai 200070, China.
authors: Xiaofang
authors: X
authors: Feng
authors: Department of Neurology, Central Hospital of Zhabei District, Shanghai 200070, China.
authors: Luojun
authors: L
authors: Wang
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects*; D001929:Brain Edema / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D020520:Brain Infarction / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D003921:Diabetes Mellitus, Experimental; D007375:Interleukin-1 / Q000378:metabolism; D017628:Microglia / Q000378:metabolism* / Q000473:pathology; D047495:PPAR gamma / Q000037:antagonists & inhibitors / Q000378:metabolism; D015230:Prostaglandin D2 / Q000031:analogs & derivatives* / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D007375:Interleukin-1; D047495:PPAR gamma; D015230:Prostaglandin D2; D014409:Tumor Necrosis Factor-alpha; C477819:15-deoxyprostaglandin J2; C539355:CD68 protein, rat; D000097382:CD68 Molecule