Biochemistry And Microbial Sciences - Research Publications

Permanent URI for this collectionhttps://kr.cup.edu.in/handle/32116/27

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    Endophytes as nature's gift to plants to combat abiotic stresses
    (Oxford University Press, 2022-12-20T00:00:00) Godara, Himanshi; Ramakrishna, Wusirika
    In recent decades, scientists have recognized that plants' distinct and immensely dynamic microbial communities are more than just "passengers,"but instead, play an important role in their development, and shielding against abiotic and biotic stresses. Endophytes comprise fungi and bacteria that live within plant tissues and support growth when plants are under stress. All plants in nature are considered to have symbiotic association with endophytes. A comprehensive review of the accessible data suggests that mobility, cell-wall degradation capacity, and reactive oxygen species scavenging are critical attributes for the successful colonization of endophytes. Plants encounter several abiotic stresses caused by climate change and global warming, which have an effect on their growth and production. Abiotic stress like high temperature, salinity, and high precipitation can severely affect plants compared to biotic stress. This review aims to highlight what role endophytes play to aid plant growth under abiotic stress conditions like heat, salinity, and drought. In the current review, we discuss how endophytic microbes can be efficiently used for the improvement and promotion of plant growth and crop production under abiotic stress conditions. � 2022 The Author(s). Published by Oxford University Press on behalf of Applied Microbiology International.
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    Neuroprotective and Neurorescue Mode of Action of Bacopa monnieri (L.) Wettst in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Parkinson�s Disease: An In Silico and In Vivo Study
    (Frontiers Media S.A., 2021-03-16T00:00:00) Singh, Babita; Pandey, Shivani; Rumman, Mohammad; Kumar, Shashank; Kushwaha, Prem Prakash; Verma, Rajesh; Mahdi, Abbas Ali
    Ethnopharmacological Relevance: Parkinson�s disease (PD) is characterized by progressive death of dopaminergic neurons. The presently used medicines only tackle the symptoms of PD, but none makes a dent on the processes that underpin the disease�s development. Herbal medicines have attracted considerable attention in recent years. Bacopa monnieri (L.) Wettst (Brahmi) has been used in Indian Ayurvedic medicine to enhance memory and intelligence. Herein, we assessed the neuroprotective role of Bacopa monnieri (L.) Wettst on Parkinson�s disease. Aim of the Study: Bacopa monnieri (L.) Wettst, a medicinal herb, is widely used as a brain tonic. We investigated the neuroprotective and neurorescue properties of Bacopa monnieri (L.) Wettst extract (BME) in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mice model of PD. Materials and Methods: The mice model of MPTP-induced PD is used in the study. In the neuroprotective (BME + MPTP) and neurorescue (MPTP + BME) experiments, the animals were administered 40�mg/kg body weight BME orally before and after MPTP administration, respectively. Effect of BME treatment was evaluated by accessing neurobehavioral parameters and levels of dopamine, glutathione, lipid peroxide, and nitrites. An in silico study was performed using AutoDock Tools 1.5.6 (ADT). Results: A significant recovery in behavioral parameters, dopamine level, glutathione level, lipid peroxides, and nitrite level was observed in BME-treated mice. Treatment with BME before or after MPTP administration has a protective effect on dopaminergic neurons, as evidenced by a significant decrease in GFAP immunostaining and expression of inducible nitric oxide synthase (iNOS) in the substantia nigra region; however, the degree of improvement was more prominent in mice receiving BME treatment before MPTP administration. Moreover, the in silico study revealed that the constituents of BM, including bacosides, bacopasides, and bacosaponins, can inactivate the enzyme monoamine oxidase B, thus preventing the breakdown of MPTP to MPP+. Conclusion: Our results showed that BME exerts both neuroprotective and neurorescue effects against MPTP-induced degeneration of the nigrostriatal dopaminergic neurons. Moreover, BME may slow down the disease progression and delay the onset of neurodegeneration in PD. � Copyright � 2021 Singh, Pandey, Rumman, kumar, Kushwaha, Verma and Mahdi.
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    Phytochemical Ginkgolide B Attenuates Amyloid-? amage and Altered Cellular Responses in Human Neuroblastoma SH-SY5Y Cells
    (IOS Press, 2017) Gill I.; Kaur S.; Kaur N.; 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-? (A?)-induced oxidative stress responses, a major cause for AD, in the undifferentiated and differentiated human neuroblastoma SH-SY5Y cells. A?1-42-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 A?1-42-induced oxidative stress was assessed. We report that the differentiated cells are highly vulnerable to A?1-42-induced oxidative stress events as exerted by the deposition of A? in AD. Results of the current study suggest that the pre-treatment of GB, followed by A?1-42 treatment for 24, displayed neuro-protective potential, which countered A?1-42-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, A?1-42 induces oxidative damage to the cellular biomolecules, which are associated with AD pathology, and are protected by the pre-treatment of GB against A?-toxicity. Taken together, this study advocates for phytochemical-based therapeutic interventions against AD.