چاپ صفحه |  صفحه نخست سامانه |  نویسندگان |  اطلاعات تفضیلی |  دانلود مقاله | دانشگاه علوم پزشکی تبریز |
| نویسنده ثبت کننده مقاله | لیلا حسینی |
| مرحله جاری مقاله | تایید نهایی |
| دانشکده/مرکز مربوطه | روانپزشکی و علوم رفتاری |
| کد مقاله | 82797 |
| عنوان فارسی مقاله | Intranasal delivery of mitochondria alleviated cognitive impairments and mitochondrial dysfunction in the photothrombotic model of mPFC stroke in mice |
| عنوان لاتین مقاله | Intranasal delivery of mitochondria alleviated cognitive impairments and mitochondrial dysfunction in the photothrombotic model of mPFC stroke in mice |
| نوع ارائه | پوستر |
| عنوان کنگره / همایش | 11th World Congress of Neuroscience |
| نوع کنگره / همایش | بین المللی |
| کشور محل برگزاری کنگره/ همایش | Spain |
| شهر محل برگزاری کنگره/ همایش | Granada |
| سال انتشار/ ارائه شمسی | 1402 |
| سال انتشار/ارائه میلادی | 2023 |
| تاریخ شمسی شروع و خاتمه کنگره/همایش | 1402/06/18 الی 1402/06/22 |
| آدرس لینک مقاله/ همایش در شبکه اینترنت | IBRO Neuroscience Reports, DOI: 10.1016/j.ibneur.2023.08.083 |
| آدرس علمی (Affiliation) نویسنده متقاضی | Research Center of Psychiatry and Behavioral Sciences, Tabriz University of Medical Sciences, Tabriz, Iran |
| نویسنده | نفر چندم مقاله |
|---|---|
| لیلا حسینی | اول |
| محمد کریمی پور | دوم |
| عنوان | متن |
|---|---|
| خلاصه مقاله | Objectives: Dysfunction in mitochondrial activity may have a profound role in ischemic stroke-induced neuronal death, hence maintaining the mitochondrial function seems to be valuable for neuronal viability and neurological improvement. Methods: C57BL/6J mice were allocated into sham and stroke groups. Mice in the stroke groups underwent photothrombotic-induced stroke in the medial prefrontal cortex (mPFC) and were divided into the following subgroups; RB, Mito 85, Mito 170, and Mito 340, and received their respective treatments via intra-nasal route every other day (3 days per week) for one week. A battery of behavioral tests including social interaction, passive avoidance, and the Lashley III maze was used to investigate social, contextual, and spatial memories. Moreover, changes in mitochondrial function, including reactive oxygen species (ROS), ATP levels, and mitochondrial membrane potential, were assessed in mPFC. The expression of growth-associated protein 43 (GAP-43), post-synaptic density-95 (PSD-95), and synaptophysin (SYP) was detected by western blotting. Results: Behavioral results revealed that mitotherapy alleviated ischemia-induced memory impairment. Also, transplantation of exogenous mitochondria lowered ROS, restored ATP generation, and improved mitochondrial membrane potential. Induction of ischemia decreased the levels of synaptic markers in mPFC while exogenous mitochondria (170 and 340mg) significantly upregulated the expression of GAP-43 and PSD-95 after ischemic stroke. Conclusion: Our research highlighted the importance of mitotherapy in regulating synaptic markers expression and mitochondria function, which could represent a potential strategy for improving cognitive and memory deficits following stroke. |
| کلمات کلیدی | Ischemic stroke. Mitotherapy. Photothrombotic stroke. Neuroprotection. Mitochondrial dysfunction. Synaptic plasticity |
| نام فایل | تاریخ درج فایل | اندازه فایل | دانلود |
|---|---|---|---|
| IBRO23.pdf | 1402/07/22 | 137638 | دانلود |
| IBRO.pdf | 1402/08/19 | 254151 | دانلود |
| IBRO23 - Leila Hosseini Signed COA.pdf | 1402/08/19 | 209329 | دانلود |
