Oxidative stress induced antioxidant and neurotoxicity demonstrated in vivo zebrafish embryo or larval model and their normalization due to morin showing therapeutic implications

氧化应激 抗氧化剂 谷胱甘肽 神经保护 药理学 谷胱甘肽还原酶 谷胱甘肽过氧化物酶 神经毒性 生物化学 脂质过氧化 莫林 活性氧 生物 化学 超氧化物歧化酶 毒性 医学 有机化学 病理
作者
Praveen Kumar Issac,Ajay Guru,Manikandan Velayutham,Raman Pachaiappan,Mariadhas Valan Arasu,Naïf Abdullah Al-Dhabi,Ki Choon Choi,Ramasamy Harikrishnan,Jesu Arockiaraj
出处
期刊:Life Sciences [Elsevier BV]
卷期号:283: 119864-119864 被引量:88
标识
DOI:10.1016/j.lfs.2021.119864
摘要

The study examined that morin as possible antioxidant and neuroprotective due to oxidative stress (H2O2) in zebrafish larval model. Zebrafish larvae were induced with oxidative stress using H2O2 at 1 mM; their behavioural changes were assessed through partition preference and horizontal compartment test. The head section without eyes and yolk sac of zebrafish larvae were employed for enzyme assays such as SOD, CAT, Thiobarbituric acid reactive substances assay, reduced glutathione, glutathione peroxidase activity, glutathione S transferase, Acetylcholinesterase activity and nitrate levels. Also, intracellular ROS and apoptosis in larval head was detected by DCFDA and acridine orange staining followed by gene expression studies. Morin exposure was not harmful to the larvae at concentration between 20 and 60 μM, but it caused non-lethal deformity between 80 and 100 μM. In the partition test, zebrafish embryos treated with H2O2 showed cognitive impairment, whereas the morin-treated groups showed an improved behavioural activity. The study also found that restoring antioxidant enzymes and reduced lipid peroxidation which had a neuroprotective impact. Inhibition of NO overproduction and increased AChE activity were also shown to reduce the neuronal damage. Apoptosis and intracellular ROS levels were reduced in larvae when it was co-incubated with morin. Morin treatment up regulated the antioxidant enzymes against oxidative stress. Morin provides protection against H2O2 induced oxidative stress through a cellular antioxidant defence mechanism by up-regulating gene expression, thus increasing the antioxidant activity at cellular or organismal stage.
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