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Echinatin mitigates sevoflurane-induced hippocampal neurotoxicity and cognitive deficits through mitigation of iron overload and oxidative stress

التفاصيل البيبلوغرافية
العنوان: Echinatin mitigates sevoflurane-induced hippocampal neurotoxicity and cognitive deficits through mitigation of iron overload and oxidative stress
المؤلفون: Zilong Xu, Yanqiu You, Qiuqin Tang, Hui Zeng, Tianshou Zhao, Juan Wang, Fujun Li
المصدر: Pharmaceutical Biology, Vol 60, Iss 1, Pp 1915-1924 (2022)
بيانات النشر: Taylor & Francis Group, 2022.
سنة النشر: 2022
المجموعة: LCC:Therapeutics. Pharmacology
مصطلحات موضوعية: Anaesthesia, postoperative cognitive dysfunction, hippocampal neuron, ferroptosis, Therapeutics. Pharmacology, RM1-950
الوصف: Context Sevoflurane (Sev) is a commonly used surgical anaesthetic; it has neurotoxic effects on the brain. Echinatin (Ech) is reported to have anti-inflammatory and antioxidant activity.Objective This research confirms the effect of Ech on Sev-induced neurotoxicity and cognitive deficits.Materials and methods Primary rat hippocampal neurons were treated with 4.1% Sev for 6 h in the presence of Ech (5, 10, and 20 μM) or vehicle, followed by a further 42 h of culture. Male Sprague-Dawley aged rats were divided into 6 groups (n = 6): control, Sev, Sev + Ech (20 mg/kg;), Sev + Ech (40 mg/kg), and Sev + Ech (80 mg/kg). Rats were intraperitoneally injected with Ech or vehicle 1 h before Sev exposure (2% Sev for 5 h).Results We found that Ech (5, 10, and 20 μM) elevated cell viability (1.29-, 1.51-, 1.68-fold) but mitigated apoptosis (23.87% vs. 16.48%, 12.72%, 9.02%), oxidative stress, and ferroptosis in hippocampal neurons with Sev treatment. Ech activated the Nrf2 expression in Sev-induced in vitro and in vivo models of anaesthetic neurotoxicity. Ech also weakened neurotoxicity in hippocampal neurons with Sev treatment by increasing Nrf2 expression level. Moreover, Ech alleviated hippocampus neurons apoptosis (19.38% vs. 16.05%, 11.71%, 8.88%), oxidative stress, and ferroptosis in rats with Sev treatment. Ech improved Sev-induced cognitive deficits in rats.Conclusions Ech alleviates Sev-induced neurotoxicity and cognitive deficits by mitigation of ferroptosis and oxidative stress. Ech may be developed as a new promising therapeutic drug for treatment of cerebral nerve injury caused by surgical anaesthesia.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 13880209
1744-5116
1388-0209
Relation: https://doaj.org/toc/1388-0209; https://doaj.org/toc/1744-5116
DOI: 10.1080/13880209.2022.2123941
URL الوصول: https://doaj.org/article/ab1c91ee54ae4d18b1ad31f724ab47d0
رقم الأكسشن: edsdoj.b1c91ee54ae4d18b1ad31f724ab47d0
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:13880209
17445116
DOI:10.1080/13880209.2022.2123941