International Research journal of Management Science and Technology

  ISSN 2250 - 1959 (online) ISSN 2348 - 9367 (Print) New DOI : 10.32804/IRJMST

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NITRIC OXIDE MODULATORY MECHANISM OF GINSENG AGAINST MILD TRAUMATIC BRAIN INJURY INDUCED COGNITIVE IMPAIREMENT

    3 Author(s):  PRAMA NAND,DR. SURAJ KUMAR,DR.AMITABH KISHORE DWIVEDI

Vol -  9, Issue- 3 ,         Page(s) : 496 - 501  (2018 ) DOI : https://doi.org/10.32804/IRJMST

Abstract

Traumatic brain injury because of accidents is thought to be a testing public health issue. It is a main source of death and inability which represents around 2.5 to 6.5 million cases in the United States. It is a typical neurological impairment known to trigger an assortment of symptoms running from straightforward headache to perpetual cognitive dysfunction. Brain injury can be named essential, which happens quickly after trauma, and secondary, which incorporates a course of wounds that develop over some stretch of time after the initial traumatic scene. Survivors of head trauma experience the ill effects of a wide assortment of pathologies, for example, neurological shortages, behavioral and emotional impairments, debilitated engine function, hostility, seizures and cognitive problems, all of which rely upon the seriousness of the injury. Head injury is known to make significant damage the hippocampal cells, which assumes a crucial role in the preparing of spatial learning and memory. A clinical report additionally demonstrates that head trauma survivor's faces trouble in spatial learning. Oxidative damage and apoptosis are two pathogenic mechanisms that assume a significant role in the movement of secondary brain injury. Damage caused by oxidative cellular injury and initiated inflammatory reaction have been notable.

1. Varki, A. (2008): Sialic acids in human health and Disease. Trends Mol. Med. 14: 351-360.
2. Sakul, A.; Cumaoglu, A.; Aydın, E.; Ar, N.; Dilsiz, N. and Karasu, C. (2013): Age- and diabetes-induced regulation of oxidative protein modification in rat brain and peripheral tissues: Consequences of treatment with antioxidant pyridoindole. Exp. Gerontol. 48: 476-484.
3. Savini, I.; Catani, M. V.; Evangelista, D.; Gasperi, V. and Avigliano, L. (2013): Obesity-associated oxidative stress: strategies finalized to improve redox state. Int. J. Mol. Sci. 14: 10497-10538.
4. Bansal, S.; Chawla, D.; Siddarth, M.; Banerjee, B. D.; Madhu, S. V. and Tripathi, A. K. (2013): A study on serum advanced glycation end products and its association with oxidative stress and paraoxonase activity in type 2 diabetic patients with vascular complications. Clin. Biochem. 46: 109-114
5. Samatha, P.; Venkateswarlu, M. and Siva Prabodh, V. (2012): Lipid Profile Levels in Type 2 Diabetes Mellitus from the Tribal Population of Adilabad in Andhra Pradesh, India. J. Clin. Diagn. Res. 6: 590-592.
6. Schiffrin, E. L. (2010): Antioxidants in Hypertension and Cardiovascular Disease, Mol. Interv. 10: 354-362.
7. Catanzaroa, O.; Capponia, J. A.; Michielia, J.; Labala, E.; Martinoa, I. D. and Sirois, P. (2013): Bradykinin B1 antagonism inhibits oxidative stress and restores Na+K+ ATPase activity in diabetic rat peripheral nervous system. Peptides. 44: 100- 104.
8. Pazdro, R. and Burgess, J. R. (2010): The role of vitamin E and oxidative stress in diabetes complications. Mech. Ageing Dev. 131: 276-286.

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