Department of Genetic Engineering and Biotechnology, Bangabandhu Sheikh Mujibur Rahman Maritime University, Dhaka, Bangladesh.
Department of Biochemistry and Molecular Biology, Faculty of Life Science, Bangabandhu Sheikh Mujibur Rahman Science and Technology University, Gopalganj 8100, Bangladesh.
Oxid Med Cell Longev. 2022 Aug 26;2022:7743705. doi: 10.1155/2022/7743705. eCollection 2022.
Molecules with at least one unpaired electron in their outermost shell are known as free radicals. Free radical molecules are produced either within our bodies or by external sources such as ozone, cigarette smoking, X-rays, industrial chemicals, and air pollution. Disruption of normal cellular homeostasis by redox signaling may result in cardiovascular, neurodegenerative diseases and cancer. Although ROS (reactive oxygen species) are formed in the GI tract, little is known about how they contribute to pathophysiology and disease etiology. When reactive oxygen species and antioxidants are in imbalance in our bodies, they can cause cell structure damage, neurodegenerative diseases, diabetes, hypercholesterolemia, atherosclerosis, cancer, cardiovascular diseases, metabolic disorders, and other obesity-related disorders, as well as protein misfolding, mitochondrial dysfunction, glial cell activation, and subsequent cellular apoptosis. Neuron cells are gradually destroyed in neurodegenerative diseases. The production of inappropriately aggregated proteins is strongly linked to oxidative stress. This review's goal is to provide as much information as possible about the numerous neurodegenerative illnesses linked to oxidative stress. The possibilities of multimodal and neuroprotective therapy in human illness, using already accessible medications and demonstrating neuroprotective promise in animal models, are highlighted. Neuroprotection and neurolongevity may improve from the use of bioactive substances from medicinal herbs like , , and Many neuroprotective drugs' possible role has been addressed. Preventing neuroinflammation has been demonstrated in several animal models.
具有最外层不成对电子的分子被称为自由基。自由基分子要么在我们体内产生,要么由外部来源产生,如臭氧、吸烟、X 射线、工业化学物质和空气污染。氧化还原信号对正常细胞内稳态的破坏可能导致心血管、神经退行性疾病和癌症。尽管 ROS(活性氧)在胃肠道中形成,但它们如何促进病理生理学和疾病病因知之甚少。当体内活性氧和抗氧化剂失衡时,它们会导致细胞结构损伤、神经退行性疾病、糖尿病、高胆固醇血症、动脉粥样硬化、癌症、心血管疾病、代谢紊乱和其他与肥胖相关的疾病,以及蛋白质错误折叠、线粒体功能障碍、神经胶质细胞激活和随后的细胞凋亡。在神经退行性疾病中,神经元细胞逐渐被破坏。不适当聚集的蛋白质的产生与氧化应激强烈相关。本综述的目的是提供尽可能多的关于与氧化应激相关的许多神经退行性疾病的信息。强调了在人类疾病中使用已经可获得的药物进行多模态和神经保护治疗的可能性,并在动物模型中显示出神经保护的潜力。使用草药中的生物活性物质,如 、 、 ,可能会改善神经保护和神经长寿。已经解决了许多神经保护药物的可能作用。已经在几种动物模型中证明了预防神经炎症的作用。
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