Department of Biomedical engineering, Fourth Military Medical University, Xi'an, China; Shaanxi Key Laboratory of Brain Disorders & School of Basic Medical Sciences, Xi'an Medical University, China.
Department of Anesthesiology, College of Stomatology, Fourth Military Medical University, Xi'an, China.
Environ Toxicol Pharmacol. 2019 Apr;67:117-123. doi: 10.1016/j.etap.2019.02.011. Epub 2019 Feb 19.
This study was designed to investigate the neuroprotective effect of hyperoxygenate hydrogen-rich saline (HOHS) against brain injury induced by carbon monoxide (CO) poisoning in rats. A rat model of CO poisoning was established by administering CO via intraperitoneal injection to male Sprague-Dawley rats. Forty-eight adult male rats were randomly divided into the following groups: normal control group (NG), CO poisoning group (CO), HOS treatment group (hyperoxygenated solution, HOS) and HOHS treatment group (HOHS). After CO poisoning, the carboxyhemoglobin (COHb) contents in the blood of rats in all the CO poisoning groups were increased significantly. However, HOS and HOHS significantly decreased COHb contents, furthermore, the HOHS group had lower COHb contents than the HOS group. Arterial oxygen partial pressure (PaO) and arterial oxygen saturation (SaO) results showed that HOS and HOHS could improve the oxygenation of the rats with CO poisoning. Compared with the CO group, the HOS group and the HOHS group had persistently neuroprotective effect on CO-induced brain injury, as assessed by modified neurological severity score (mNSS), furthermore, the HOHS group had better neurological functional recovery than the HOS group. The neuronal apoptosis induced by CO was also evaluated. Except the NG group, all the CO-poisoning groups had varying degrees of neuronal apoptosis. There was lesser degree of neuronal apoptosis in both the HOS group and the HOHS group than that in the CO group. Moreover, the HOHS group had more minor degree of neuronal apoptosis than the HOS group. Compared with the CO group, the free radicals production in the HOS group and the HOHS group were significantly inhibited. In addition, there were significantly difference in the free radicals production between the HOS group and the HOHS group. We could conclude that HOHS exerted a stronger neuroprotective effect against CO-induced brain injury than HOS, and the neuroprotective mechanism of HOHS may be related with inhibition of both neuronal apoptosis and free radicals.
本研究旨在探讨高氧含氢生理盐水（HOHS）对一氧化碳（CO）中毒诱导的大鼠脑损伤的神经保护作用。通过腹腔注射 CO 建立大鼠 CO 中毒模型。将 48 只成年雄性 Sprague-Dawley 大鼠随机分为以下几组：正常对照组（NG）、CO 中毒组（CO）、高氧溶液组（HOS）和 HOHS 治疗组（HOHS）。CO 中毒后，所有 CO 中毒组大鼠血液中的碳氧血红蛋白（COHb）含量均显著增加。然而，HOS 和 HOHS 可显著降低 COHb 含量，此外，HOHS 组的 COHb 含量低于 HOS 组。动脉血氧分压（PaO）和动脉血氧饱和度（SaO）结果表明，HOS 和 HOHS 可改善 CO 中毒大鼠的氧合作用。与 CO 组相比，HOS 组和 HOHS 组对 CO 诱导的脑损伤具有持续的神经保护作用，通过改良神经功能缺损评分（mNSS）评估，此外，HOHS 组的神经功能恢复优于 HOS 组。还评估了 CO 诱导的神经元凋亡。除 NG 组外，所有 CO 中毒组均有不同程度的神经元凋亡。HOS 组和 HOHS 组的神经元凋亡程度均低于 CO 组。此外，HOHS 组的神经元凋亡程度比 HOS 组更轻微。与 CO 组相比，HOS 组和 HOHS 组的自由基生成明显受到抑制。此外，HOS 组和 HOHS 组之间的自由基生成也有显著差异。与 CO 组相比，HOS 组和 HOHS 组的自由基生成明显受到抑制。此外，HOS 组和 HOHS 组之间的自由基生成也有显著差异。我们可以得出结论，HOHS 对 CO 诱导的脑损伤的神经保护作用强于 HOS，HOHS 的神经保护机制可能与抑制神经元凋亡和自由基生成有关。
