Objective_To investigate the effect of estrogen(E2) on different age rat groups of Parkinson’s disease (PD) models induced by Rotenone and its mechanism.Methods_24-month-old SD rats(high age group)and 12-week-age SD rats( low age group ) were divided into control group ( saline ) , Rotenone treatment group ( Rotenone 2 mg/kg), Estrogen treatment group(Rotenone 2 mg/kg and E2 1 mg/kg)and Tamoxifen treatment group(Rote-none 2 mg/kg, E2 1 mg/kg and Tamoxifen 1 mg/kg).Behavior tests were carried out to observe the change of movement function, Immunohistochemistry and Western blot were used to assess the changes of TH and LC-3. HPLC-ECD was used to detect possible changes of monoamine neurotransmitters in striatum.Results_1) Rotenone reduced significantly old age rat’s rotarod latencies and prolonged the climbing pole time(P<0.05).E2 ameliorated this effect, Tamoxifen reduced the effect of E2.2) Rotenone significantly reduced the number of TH positive cells in
high age rats(P<0.05), E2 partly restored TH positive cell loss, Tamoxifen reduced this effect of E2, so did the ex-pression of TH protein.3)Rotenone increased the expression of LC-3(P<0.05), E2 did not affect the expression of LC-3, so did Tamoxifen.4)Rotenone significantly decreased the level of DA and its metabolite DOPAC(P<0.05), elevated the level of 5-HT especially in old rats(P<0.05).E2 downregulated the influence, and Tamoxifen reduced the effect of E2.5)Rotenone increased the number of autophagosomes, but E2 increased the proportion of autolyso-somes/autophagosomes.Conclusions_Old age rat PD model was more reliable.Estrogen promoted autophagy ma-ture, and had obvious therapeutic effect on rat PD model induced by rotenone.

Ferroptosis is a new type of programmed cell death that is closely associated with the pathophysiological process of ischemic stroke. Ferroptosis inhibitors can improve neurological function and provide neuroprotection after cerebral ischemia. Therefore, the role of ferroptosis in ischemic stroke and the regulation of ferroptosis to intervene in the occurrence and development of ischemic stroke have become a research hotspot. This article reviews the molecular mechanism and potential therapeutic targets of ferroptosis during ischemic stroke, hoping to provide new perspectives for the treatment of ischemic stroke.