運動和S-亞硝基穀胱甘肽的組合可改善中風的恢復(Combination of exercise and S-nitrosoglutathione improves recovery from stroke)



運動和S-亞硝基穀胱甘肽的組合可改善中風的恢復

在最新一期的修復神經病學和神經科學雜誌上發表的一項研究中,科學家報告說,將運動與神經血管保護劑S-亞硝基穀胱甘肽(GSNO)相結合的療法可以改善大鼠模型中風的恢復。 GSNO是一種天然存在於體內的化合物,沒有已知的副作用或毒性。

“在我們的研究中,GSNO或運動鍛煉提供神經保護,減少神經細胞死亡,維持組織結構,並通過刺激神經元修復介質的表達來輔助功能恢復,”醫學大學的首席研究員Avtar K. Singh博士說。南卡羅來納州(MUSC)和拉爾夫H.約翰遜VA醫療中心,查爾斯頓。 “GSNO與運動相結合,加快了速度,提高了恢復的程度。”

中風既是急性疾病,也是慢性病。雖然急性期與細胞死亡和繼發性損傷有關,但慢性期的特徵在於神經修復機制不足。大多數單藥治療失敗是因為藥物在慢性期無效。康復已被用於改善慢性期的神經功能,但其療效緩慢且有限。理想的療法可以改善兩個階段的損傷,因此包括康復和提供神經保護和修復的藥物(如GSNO)的組合。

辛格博士及其來自MUSC的同事(Drs.Mushfiquddin Khan,Harutoshi Sakakima和Inderjit Singh)在大鼠中誘發中風,然後將其分配到五個治療組中的一個。第一組未接受任何治療;第二組接受運動治療;第三組與GSNO;第四組接受運動和GSNO治療;第五組接受假治療。在運動處理中,要求大鼠每天以恆定速度在旋轉桿電動機單元上運行20分鐘。在整個治療期間施用GSNO。

在手術前後評估每組動物的神經功能,運動行為和運動功能。 測量梗塞的大小。 誘導中風後第7天和第14天,取出腦組織樣品並進行測試。

施用GSNO不僅可以減少腦損傷,還可以改善神經學評分。 單獨運動不能顯著減少梗塞體積,因為運動在手術後72小時開始,並且在此之前發生梗塞。 然而,運動確實改善了神經行為功能。 結合治療具有協同效應,並且提供比GSNO或單獨運動更大的功能改善。

對腦組織的分析發現,GSNO可加速神經和運動功能的恢復,並通過刺激神經營養因子BDNF及其受體的表達來增強運動的益處,神經營養因子BDNF及其受體在神經修復過程中發揮關鍵作用,並通過激活Akt,一種蛋白質參與 在細胞增殖。 辛格博士和她的合作者Drs。 Mushfiquddin Khan和Inderjit Singh得出結論:“GSNO是一個有吸引力的候選者,可以在人類中進行神經修復和中風後的康復治療。”




Combination of exercise and S-nitrosoglutathione improves recovery from stroke



In a study published in the current issue of Restorative Neurology and Neuroscience scientists report that a therapy combining exercise with the neurovascular protective agent S-nitrosoglutathione (GSNO) improved recovery from stroke in a rat model. GSNO is a compound found naturally in the body and it has no known side effects or toxicity.



"In our study, GSNO or motor exercise provided neuroprotection, reduced neuronal cell death, maintained tissue structure, and aided functional recovery by stimulating the expression of neuronal repair mediators," says lead investigator Avtar K. Singh, MD, of the Medical University of South Carolina (MUSC) and the Ralph H. Johnson VA Medical Center, Charleston. "GSNO in combination with exercise accelerated the rate and enhanced the degree of recovery."



Stroke is both an acute disease and a chronic condition. While the acute phase is associated with cell death and secondary injury, the chronic phase is characterized by insufficient neurorepair mechanisms. Most monotherapies fail because the drugs are not effective in the chronic phase. Rehabilitation has been used to improve neurofunction in the chronic phase, but its efficacy is slow and limited. An ideal therapy would ameliorate the injury in both phases and therefore include a combination of rehabilitation and an agent that provides both neuroprotection and repair, such as GSNO.


Dr. Singh and her colleagues from MUSC (Drs. Mushfiquddin Khan, Harutoshi Sakakima and Inderjit Singh) induced stroke in rats, which were then assigned to one of five treatment groups. The first group received no treatment; the second group was treated with exercise; the third group with GSNO; the fourth group received both exercise and GSNO treatment; and the fifth group received a sham treatment. In the exercise treatment, rats were required to run on a rotating rod motor unit at a constant speed for 20 minutes a day. GSNO was administered throughout the treatment period.



Animals in each group were evaluated for neurological function, motor behavior, and locomotor function before and after the procedure. The size of the infarct was measured. At 7 and 14 days after stroke was induced, brain tissue samples were removed and tested.



Administration of GSNO not only reduced brain injury but also improved neurological scores. Exercise alone could not significantly reduce infarct volume, because the exercise started 72 hours post procedure and infarctions occur before then. However, exercise did improve neurobehavioral functions. Combining the therapies had a synergistic effect, and provided greater functional improvement than either GSNO or exercise alone.


Analysis of the brain tissue found that GSNO accelerates the recovery of neurological and motor functions and enhances the benefit of exercise by stimulating the expression of neurotrophic factor BDNF and its receptors, which play critical roles in neurorepair processes, and by activating Akt, a protein involved in cell proliferation. Dr. Singh and her collaborators Drs. Mushfiquddin Khan and Inderjit Singh conclude, "GSNO is an attractive candidate to be investigated in humans for neurorepair and rehabilitation following stroke."

Source:

Restorative Neurology and Neuroscience

#GSNO #天然誓約
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