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Your search keyword '"Ran, Jihua"' showing total 3 results
Start Over Author "Ran, Jihua" Topic apoptosis
3 results on '"Ran, Jihua"'

1. Oral administration of Ginkgolide B alleviates hypoxia-induced neuronal damage in rat hippocampus by inhibiting oxidative stress and apoptosis

Author

Wang Li, Shi Qinghai, Li Kai, Ma Xue, Niu Lili, Ran Jihua, Liu Zhengxiang, Li Xiaoling, Ge Di, Yang Qi, Deng Mengyun, and Fu Jianfeng

Subjects
Apoptosis, Ginkgolide B, Hippocampus, Hypoxia, Oxidative stress injury, Medicine
Abstract

Objective(s): The aim of this study is to explore the potential neuroprotective effects of Ginkgolide B (GB), a main terpene lactone and active component in Ginkgo biloba, in hypoxia-induced neuronal damage, and to further investigate its possible mechanisms.Materials and Methods: 54 Sprague-Dawley rats were randomly divided into three groups: the untreated control group (n=18); the hypoxia group (n=18; exposed to 6000 m simulated plateau altitude for six days); and the GB group (n=18; intragastric administration of 12 mg/kg GB three days prior to rapid adaption to 6000 m and on the first two days of hypoxia). After hypoxia exposure for six days, we dissected out the brain hippocampi and performed hematoxylin and eosin staining, Nissl staining, and TUNEL staining. Homogenates of the hippocampi were used to test the oxidative stress indices including malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), and catalase. Bax and caspase-3 expression in the hippocampal tissue was measured using qRT-PCR.Results: Treatment with GB before exposure to hypoxia could protect neural cells and increase the number of Nissl bodies. TUNEL and qRT-PCR results demonstrated that GB treatment could decrease apoptotic cells in different areas of the hippocampus. Antioxidant defense systems such as SOD, GSH, and catalase were decreased (P

Published
2019
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3. 1400 W ameliorates acute hypobaric hypoxia/reoxygenation-induced cognitive deficits by suppressing the induction of inducible nitric oxide synthase in rat cerebral cortex microglia

Author

Ran Jihua, Xin Liu, Ning Wang, Liu Zhengxiang, Jianfeng Fu, Qinghai Shi, Jiang Zheng, and Xinchuan Zheng

Subjects
0301 basic medicine, Nitric Oxide Synthase Type II, Apoptosis, Nerve Tissue Proteins, Pharmacology, Nitric Oxide, medicine.disease_cause, Nitric oxide, Rats, Sprague-Dawley, 03 medical and health sciences, Behavioral Neuroscience, chemistry.chemical_compound, 0302 clinical medicine, Enos, Malondialdehyde, medicine, Animals, Annexin A5, Hypoxia, Maze Learning, Cells, Cultured, biology, Microglia, Hypoxia (medical), biology.organism_classification, Rats, Oxygen, Nitric oxide synthase, Disease Models, Animal, 030104 developmental biology, medicine.anatomical_structure, Gene Expression Regulation, chemistry, Cerebral cortex, Immunology, biology.protein, Tyrosine, Imines, Lipid Peroxidation, medicine.symptom, Cognition Disorders, 030217 neurology & neurosurgery, Oxidative stress
Abstract

Nitric oxide (NO) is involved in neuronal modifications, and overproduction of NO contributes to memory deficits after acute hypobaric hypoxia-reoxygenation. This study investigated the ability of the iNOS inhibitor 1400W to counteract spatial memory deficits following acute hypobaric hypoxia-reoxygenation, and to affect expression of NOS, NO, 3-NT and MDA production, and apoptosis in rat cerebral cortex. We also used primary rat microglia to investigate the effect of 1400W on expression of NOS, NO, 3-NT and MDA production, and apoptosis. Acute hypobaric hypoxia-reoxygenation impaired spatial memory, and was accompanied by activated microglia, increased iNOS expression, NO, 3-NT and MDA production, and neuronal cell apoptosis in rat cerebral cortex one day post-reoxygenation. 1400W treatment inhibited iNOS expression without affecting nNOS or eNOS. 1400W also reduced NO, 3-NT and MDA production, and prevented neuronal cell apoptosis in cerebral cortex, in addition to reversing spatial memory impairment after acute hypobaric hypoxia-reoxygenation. Hypoxia-reoxygenation activated primary microglia, and increased iNOS and nNOS expression, NO, 3-NT, and MDA production, and apoptosis. Treatment with 1400W inhibited iNOS expression without affecting nNOS, reduced NO, 3-NT and MDA production, and prevented apoptosis in primary microglia. Based on the above findings, we concluded that the highly selective iNOS inhibitor 1400W inhibited iNOS induction in microglial cells, and reduced generation of NO, thereby mitigating oxidative stress and neuronal cell apoptosis in the rat cerebral cortex, and improving the spatial memory dysfunction caused by acute hypobaric hypoxia-reoxygenation.

Published
2017

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