ArticleSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition2025
[Effects of Inhibiting the NKCC1/AQP4 Pathway on Neurological Injury Improvement in a Rat Model of High-Altitude Cerebral Edema].
Article in Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: To investigate the pathogenesis of high-altitude cerebral edema (HACE) and develop new therapeutic strategies. Methods: Male Sprague-Dawley (SD) rats of 6 weeks old were selected and placed in a hypobaric chamber. The rats were exposed to the high-altitude environment of 7000 m above sea level for 3 days for HACE modeling. Whether the HACE model was successfully established in the rats was evaluated by measuring brain water content, the degree of disruption to the blood-brain barrier (BBB), and brain tissue Nissl staining. The experimental animals were divided into four groups, with 28 rats in each group. The blank control group was exposed to a normobaric and normoxic environment simulating the conditions at 500 m above sea level for 3 d. The other groups, including a model group (the HACE group), a bumetanide group (the positive control group), and a XH-6003 treatment group, were placed at an altitude of 7000 m above sea level and were injected with normal saline, bumetanide, and XH-6003, a new type of Na-K-2Cl cotransporter 1 (NKCC1) inhibitor, via the tail vein, respectively, twice daily for 3 d. The experimental animals were taken out of the hypobaric chamber for testing after 3 d. The primary outcome measures included brain water content, BBB permeability, changes in brain tissue morphology, and the expression levels of aquaporin-4 (AQP4) and NKCC1. The secondary outcome measures included behavioral changes, apoptosis, and oxidative stress markers. Results: The HACE rat model was successfully established. The model group exhibited increased brain water content ( Conclusion: HACE is associated with the activation of the NKCC1/AQP4 pathway. Inhibition of this pathway alleviates brain edema, BBB disruption, and neuronal and glial cell damage. These findings suggest that XH-6003 holds potential as a therapeutic strategy for HACE at the cellular and molecular levels, but its effects in improving HACE-related behavioral disorders warrant further investigation.
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