General Research Model: rat

Effects of hydrogen-rich water on the expression of aquaporin 1 in the cerebral cortex of rat with traumatic brain injury

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Hydrogen-Rich Water: A Potential Game-Changer for Traumatic Brain Injury Recovery

A 2016 study found that hydrogen-rich water increased the expression of aquaporin 1 in rats with traumatic brain injury, which may help reduce brain swelling and promote recovery. This promising finding suggests that hydrogen-rich water could be a useful tool in TBI treatment. More research is needed to confirm these results in humans, but the potential benefits are exciting.

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Abstract

Publish Year 2016 Country China Rank Positive Journal Chinese Critical Care Medicine Primary Topic Brain Secondary TopicTraumatic Brain Injury Model Rat Tertiary TopicEdema Vehicle Water (Dissolved) pH Neutral Application Injection Comparison Complement

Methods

Results: ① All rats in sham operation group had a NSS of zero at each time point. NSS of TBI group was obviously raised with time prolongation, and peaked at 24 hours followed by a lower tendency, while the score in H group was significantly lower than that of TBI group, and the difference was the most obvious at 24 hours as compared with TBI group (9.83 ± 2.78 vs.13.50± 2.42,P < 0.05).② It was shown by light microscope that in the TBI group there were pathological changes in cerebral cortex, including obvious irregular arrangement of nerve cells, cerebral edema, obvious bleeding, especially at 24 hours, then the cerebral edema became vanished gradually; and the positive expression of AQP1 in the pia mater at all the time points in the TBI group was significantly increased, and it was most obvious at 24 hours. Compared with TBI group, the pathological changes at time points of 12 hours to 5 days in H group was significantly lessened, and the positive expression of AQP1 in the cerebral pia mater was reduced obviously.③ Compared with sham operation group, the mRNA and protein expressions of AQP1 in cerebral cortex in TBI group were significantly elevated, peaked at 24 hours [AQP1 mRNA (2-△△Ct):7.50±0.26 vs.1,AQP1 protein (gray value):1.986±0.110 vs.0.336±0.034, both P < 0.05], then they gradually declined. The mRNA and protein expressions of AQP1 in cerebral cortex were significantly decreased after hydrogen-rich water treatment [24-hour AQP1 mRNA (2-△△Ct):5.40±0.21 vs.7.50±0.26, 24-hour AQP1 protein (gray value): 1.246±0.137 vs.1.986±0.110, both P < 0.05]. Conclusions: The up-regulation of AQP1 mRNA and protein in rats' cerebral cortex after TBI perhaps participates in edema formation which might be involved in the pathophysiology of cerebral edema in TBI. Early treatment with an intraperitoneally injection of hydrogen-rich water is capable of attenuating the extent of TBI-induced up-regulation of AQP1 mRNA and protein, alleviating cerebral edema, and achieving its protective effects.