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Subject: search.filters.subject.Ginkgolide B

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    Phytochemical ginkgolide b protects cultured neuroblastoma SH-SY5Y cells against a?(25-35) induced oxidative stress responses by maintaining the mitochondrial integrity
    (Rasayan Journal of Chemistry, c/o Dr. Pratima Sharma, 2020) Kaur, N; Kaur, S; Saini, M; Dhiman, M; Mantha, A.K.
    Alzheimer�s disease is associated with oxidative stress induced by accumulation of A? peptide, by disrupting the mitochondrial function. In this study, the oxidative stress responses induced by A?(25-35) and protective effects of diterpenoid phytochemical Ginkgolide B (GB) were evaluated by the determination of cellular oxidant/antioxidant status, oxidative DNA base damage and repair capacity of cells through evaluation of mitochondrial BER pathway status and the multifunctional enzyme APE1 in human neuroblastoma SH-SY5Y cells, and evaluation of mitochondrial membrane potential and changes in apoptotic pathway. It was found that A?(25-35) treatment increased ROS/RNS production, increased the activities of antioxidant SOD and Catalase enzymes, decreased the expression of mitochondrial SOD (SOD2), induced oxidative DNA base damage, might be altered the repair capacity as analyzed by the transcriptional and translational expression of APE1 and other BER pathway enzymes in the mitochondria, disrupted the mitochondrial membrane potential and induced apoptosis as a result of these responses. Phytochemical modulation by the pre-treatment of GB for 3 hr followed by the treatment of A?(25-35) for a period of 24 hr caused decrease in ROS/RNS, increase in activities of antioxidant enzymes and expression of SOD2, decreased oxidative DNA base damage and increased transcriptional and translational expression of APE1, increased/restored expression of APE1 and polymerase gamma (?) in the mitochondria, restored mitochondrial membrane potential and rescued the SH-SY5Y cells from mitochondrial-mediated apoptosis against A?(25-35) induced oxidative stress responses. Taken together, GB showed neuroprotection by restoring cellular antioxidant defense system, repair capacity of cells and restoring mitochondrial integrity (genome and membrane potential), thus rescuing the SH-SY5Y cells from A?(25-35) induced oxidative stress responses. � RAS?YAN. All rights reserved.
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    Phytochemical Ginkgolide B Attenuates Amyloid-␤ 1 - 42 Induced Oxidative Damage and Altered Cellular Responses in Human Neuroblastoma SH-SY5Y Cells
    (IOS Press, 2017) Gill, Iqbal; Kaur, Sukhchain; Kaur, Navrattan; Dhiman, Monisha; Mantha, Anil K.
    Oxidative stress is an upsurge in reactive oxygen/nitrogen species (ROS/RNS), which aggravates damage to cellular components viz. lipids, proteins, and nucleic acids resulting in impaired cellular functions and neurological pathologies including Alzheimer's disease (AD). In the present study, we have examined amyloid-β (Aβ)-induced oxidative stress responses, a major cause for AD, in the undifferentiated and differentiated human neuroblastoma SH-SY5Y cells. Aβ1-42-induced oxidative damage was evaluated on lipids by lipid peroxidation; proteins by protein carbonyls; antioxidant status by SOD and GSH enzyme activities; and DNA and RNA damage levels by evaluating the number of AP sites and 8-OHG base damages produced. In addition, the neuro-protective role of the phytochemical ginkgolide B (GB) in countering Aβ1-42-induced oxidative stress was assessed. We report that the differentiated cells are highly vulnerable to Aβ1-42-induced oxidative stress events as exerted by the deposition of Aβ in AD. Results of the current study suggest that the pre-treatment of GB, followed by Aβ1-42 treatment for 24 h, displayed neuro-protective potential, which countered Aβ1-42-induced oxidative stress responses in both undifferentiated and differentiated SH-SY5Y neuronal cells by: 1) hampering production of ROS and RNS; 2) reducing lipid peroxidation; 3) decreasing protein carbonyl content; 4) restoring antioxidant activities of SOD and GSH enzymes; and 5) maintaining genome integrity by reducing the oxidative DNA and RNA base damages. In conclusion, Aβ1-42 induces oxidative damage to the cellular biomolecules, which are associated with AD pathology, and are protected by the pre-treatment of GB against Aβ-toxicity. Taken together, this study advocates for phytochemical-based therapeutic interventions against AD.