| Autor: |
Shahraki, Jafar, Tabrizian, Kaveh, Rezaee, Ramin, Tashakori, Behnam, Dadrezaei, Seyedehzahra, Ghorani, Vahideh, Bagheri, Gholamreza, Jahantigh, Hosseinali, Hashemzaei, Mahmoud |
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| Zdroj: |
Naunyn-Schmiedeberg's Archives of Pharmacology; Oct2024, Vol. 397 Issue 10, p7673-7681, 9p |
| Abstrakt: |
Carbon monoxide (CO) is produced via incomplete combustion of fossil fuels and it may cause long-term neurological sequel upon exposure. Hesperidin (HES), a flavanone glycoside found in citrus plants, exerts diverse beneficial health effects. The present study mechanistically examined the neuroprotective effects of HES in CO-poisoned rats. Thirty male Wistar rats (five groups of six animals) were exposed to 3000 ppm CO for 1 h. Immediately after the exposure and on the next 4 consecutive days (totally five doses), rats intraperitoneally received either normal saline (the control group) or different doses of HES (25, 50, and 100 mg/kg). A sham group that was not exposed to CO was also considered. After evaluation of spatial learning and memory using a Morris water maze (MWM), animals were sacrificed and oxidative stress status in blood samples, and Akt, Bax, Bcl2, and brain-derived neurotrophic factor (BDNF) expression in brain samples were assessed. Western blot analysis indicated increased Akt but decreased Bax/Bcl2 levels in the HES 100 mg/kg, and induced BDNF levels in all HES-treated groups. MWM results showed that HES significantly decreased memory loss. The current findings indicate that HES could alleviate neurological impairments induced by CO in rats. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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