許多的文獻報告指出，抗氧化物質在動物面對氧化壓力傷害具有神經保護的效果。過去的研究指出，施予抗氧化物質如褪黑激素或綠茶素等，能降低大鼠結狀神經節內神經元因急性缺氧傷害引發的一氧化氮合成酶反應，並對神經元提供保護作用。生化學研究指出維生素C (vitamin C，主要組成物為抗壞血酸ascorbic acid) 此種抗氧化物質能清除組織間自由基，達到抗氧化的功能。維生素C為最常被廣泛研究的抗氧化物質之一，此外它在日常生活中容易取得且可自由攝取。已知一氧化氮為自由基家族的一員，除了正常生理功能中做為神經傳導物之外，其在氧化壓力傷害中經常扮演破壞者的角色。由於一氧化氮係由一氧化氮合成酶所生成，因此本實驗使用Nicotinamide adenine dinucleotide phosphate- diaphorase (NADPH-d) 組織化學染色法及神經性一氧化氮合成酶免疫組織化學染色法來檢測結狀神經節中一氧化氮合成酶的活性表現。本實驗發現缺氧後對大鼠施予維生素C可降低大鼠結狀神經節內NADPH-d/NOS的表現，此結果顯示維生素C可降低缺氧所引起的氧化壓力以及細胞傷害。我們推斷維生素C可作為有效清除自由基的營養物。 Many reports have been demonstrated that antioxidants have the neuroprotective efficiencies when animals facing the oxidative stress insults. Previous study has shown that antioxidants such as melatonin or EGCG can attenuate the NAPH-d/NOS expression which up-regulated by acute hypoxic injury in the nodose ganglion neurons of rats. Biochemical studies also have revealed that vitamin C (ascorbic acid) has pro-oxidant and antioxidant properties. Vitamin C has been one of the most-well-researched antioxidant substances, and is easy to obtain from the daily life. Nitric oxide (NO) is a member of the free radicals. Not only being a neurotransmitter in normal physiological function, it also acts as destroyer in oxidative stress injury. Since NO is generated from nitric oxide synthase (NOS), Nicotinamide adenine dinucleotide phosphate- diaphorase (NADPH-d) histochemistry and neuronal nitric oxide synthase (nNOS) immunohistochemistry were used to assess the neuronal NADPH-d/NOS reactivity in the NG. This study revealed that post-treatment of vitamin C after hypoxic insults could attenuate the expression of NADPH-d/NOS in the nodose ganglion of the rats, this indicated that vitamin C may diminish the oxidative stress and cell damage following hypoxic insults. It is therefore suggested that vitamin C may serve as a potential nutrition on quenching free radicals.
