Abstract

The biochemical indicators of wistar rat under low oxygen concentration, such as brain water content, necrosis, lactic acid and Na+-K+-ATPase, was detected to evaluate normobaric hypoxia-induced brain damage and to investigate the mechanism of wistar rat brain injury. Histopathological changes in brain tissue induced by hypoxia were investigated via hematoxylin and eosin stain (HE). Hypoxia induced factor-1α (HIF-1α) expression in brain was confirmed using immunohistochemistry. The results showed that the level of lactic acid was positively correlated with the degree of hypoxia, while concentration-dependent decrease in total Na+-K+-ATPase activity was observed. Compared with the control group, hypoxia group had a significant difference on brain water content under severe hypoxic conditions, the rate of brain necrosis increased obviously, followed by the increase of lactic acid level and the decrease of Na+-K+-ATPase activity. Histopathological analysis of brain confirmed that there was neuronal cell death in hippocampal gyrus. HIF-1α expression enhanced the hypoxia adaptation capability of the rat model through regulating the expressions of multiple genes. Lactic acid, Na+-K+-ATPase and HIF- 1α played an important role in brain injury as a possible mechanism.

Highlights

  • Hypoxia is an important pathobiological process in many diseases and causes changing of body functions [1,2]

  • The results showed that the level of lactic acid was positively correlated with the degree of hypoxia, while concentration-dependent decrease in total Na+-K+-ATPase activity was observed

  • The values of lactic acid are positively correlated with the degree of hypoxia, while total Na+-K+-ATPase activity shows a concentration-dependent decrease

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Summary

Introduction

Hypoxia is an important pathobiological process in many diseases and causes changing of body functions [1,2]. Hypoxia environment emerges quickly after appreciably long time. Hypoxia might lead to functional impairment, disturbance of consciousness, reaction dullness, retardation at action, damage of learning-memory function. Serious hypoxia might cause pathological damage or even death. Study on hypoxia mostly concentrated on hypoxic-ischemic encephalopathy (HIE) [3,4], plateau hypoxia [5,6], learning-memory [7]; therapy of various diseases induced by hypoxia and mechanisms [8,9], etc. Some studies had upgraded to cell and molecular level

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