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Effects of ranitidine on brain edema and neuroinflammatory markers in rats with traumatic brain injury
Rasyid A.W.
Chirurgia Turin
Q4Abstract
BACKGROUND: Traumatic brain injury (TBI) is one of the most frequent causes of disability and death in emergency patients. Secondary injury resulting in brain edema and increased intracranial pressure is a major TBI problem. One major cause of secondary injury is neuroinflammatory mechanisms, which are believed to be attenuated by the antihistamine ranitidine. Therefore, this study assessed the effects of ranitidine hydrochloride injection on brain edema and tumor necrosis factor-alpha (TNF-α) levels in Wistar rats with TBI.METHODS: This study used a true-experimental method with a pre- and post-test control design. Twenty-seven adult male Wistar rats were divided into trauma groups treated with (R) and without (Q) ranitidine and the control group (C). The rat TBI model was created using Marmarou’s weight-drop model. Ranitidine’s effects on histopathological brain edema extent and serum TNF-α levels were assessed 1- and 8-hours post-injury.RESULTS: Serum TNF-α levels were significantly elevated in both trauma groups (P<0.05), with significantly greater increase in the Q than in the R group. The extent of edema was significantly lower in the R than in the Q group 8 hours post-TBI (P<0.05).CONCLUSIONS: These results indicate that ranitidine significantly reduces brain edema and pro-inflammatory cytokines after TBI. This proves that ranitidine can react directly to TNF-α thereby inhibiting the inflammatory process of the blood brain barrier which can worsen neuronal dysfunction.