Abstract：
BACKGROUND: Oxidative stress is the main cause of many diseases, but because of its complex pathogenic factors, there is no clear method for treating it. Ginseng total saponin (GTS) an important active ingredients in Panax ginseng C.A. Mey (PG) and has potential therapeutic ability for oxidative stress due to various causes. However, the molecular mechanism of GTS in the treating oxidative stress damage in red blood cells (RBCs) is still unclear.
OBJECTIVE: This study aimed to examine the protective effect of GTS on RBCs under oxidative stress damage and to determine its potential mechanism.
METHODS: The oxidative stress models of rat RBCs induced by hydrogen peroxide (H2O2) and exhaustive swimming in vivo and in vitro was used. We determined the cell morphology, oxygen carrying capacity, apoptosis, antioxidant capacity, and energy metabolism of RBCs. The effect of tyrosine phosphorylation (pTyr) of Band 3 protein on RBCs glycolysis was also examined.
RESULTS: GTS reduced the hemolysis of RBCs induced by H2O2 at the lowest concentration. Moreover, GTS effectively improved the morphology, enhanced the oxygen carrying capacity, and increased antioxidant enzyme activity, adenosine triphosphate (ATP) levels, and adenosine triphosphatase (ATPase) activity in RBCs. GTS also promoted the expression of membrane proteins in RBCs, inhibited pTyr of Band 3 protein, and further improved glycolysis, restoring the morphological structure and physiological function of RBCs.
CONCLUSIONS: This study shows, that GTS can protect RBCs from oxidative stress damage by improving RBCs morphology and physiological function. Changes in pTyr expression and its related pTyr regulatory enzymes before and after GTS treatment suggest that Band 3 protein is the main target of GTS in the treating endogenous and exogenous oxidative stress. Moreover, GTS can enhance the glycolytic ability of RBCs by inhibiting pTyr of Band 3 protein, thereby restoring the function of RBCs.
OBJECTIVE: This study aimed to examine the protective effect of GTS on RBCs under oxidative stress damage and to determine its potential mechanism.
METHODS: The oxidative stress models of rat RBCs induced by hydrogen peroxide (H2O2) and exhaustive swimming in vivo and in vitro was used. We determined the cell morphology, oxygen carrying capacity, apoptosis, antioxidant capacity, and energy metabolism of RBCs. The effect of tyrosine phosphorylation (pTyr) of Band 3 protein on RBCs glycolysis was also examined.
RESULTS: GTS reduced the hemolysis of RBCs induced by H2O2 at the lowest concentration. Moreover, GTS effectively improved the morphology, enhanced the oxygen carrying capacity, and increased antioxidant enzyme activity, adenosine triphosphate (ATP) levels, and adenosine triphosphatase (ATPase) activity in RBCs. GTS also promoted the expression of membrane proteins in RBCs, inhibited pTyr of Band 3 protein, and further improved glycolysis, restoring the morphological structure and physiological function of RBCs.
CONCLUSIONS: This study shows, that GTS can protect RBCs from oxidative stress damage by improving RBCs morphology and physiological function. Changes in pTyr expression and its related pTyr regulatory enzymes before and after GTS treatment suggest that Band 3 protein is the main target of GTS in the treating endogenous and exogenous oxidative stress. Moreover, GTS can enhance the glycolytic ability of RBCs by inhibiting pTyr of Band 3 protein, thereby restoring the function of RBCs.
摘要：
背景：氧化应激是许多疾病的主要原因，但是由于其复杂的致病因素，没有明确的治疗方法。人参总皂苷（GTS）是人参C.A.Mey（PG）中的重要活性成分，对各种原因引起的氧化应激具有潜在的治疗能力。然而,GTS治疗红细胞氧化应激损伤的分子机制尚不清楚。
目的：本研究旨在探讨GTS对氧化应激损伤下红细胞的保护作用及其可能的机制。
方法：采用过氧化氢（H2O2）和力竭游泳诱导的大鼠红细胞体内和体外氧化应激模型。我们确定了细胞形态，携氧能力，凋亡，抗氧化能力，和红细胞的能量代谢。还检查了Band3蛋白的酪氨酸磷酸化（pTyr）对RBC糖酵解的影响。
结果：GTS降低了最低浓度的H2O2诱导的红细胞溶血。此外，GTS有效地改善了形貌，增强了载氧能力，和增加抗氧化酶的活性，三磷酸腺苷（ATP）水平，和红细胞中的腺苷三磷酸酶（ATPase）活性。GTS还促进RBC中膜蛋白的表达，抑制Band3蛋白的pTyr，进一步改善糖酵解，恢复红细胞的形态结构和生理功能。
结论：这项研究表明，GTS可以通过改善红细胞形态和生理功能来保护红细胞免受氧化应激损伤。GTS处理前后pTyr表达及其相关pTyr调节酶的变化提示Band3蛋白是GTS治疗内源性和外源性氧化应激的主要靶点。此外，GTS可以通过抑制Band3蛋白的pTyr来增强红细胞的糖酵解能力，从而恢复红细胞的功能。
目的：本研究旨在探讨GTS对氧化应激损伤下红细胞的保护作用及其可能的机制。
方法：采用过氧化氢（H2O2）和力竭游泳诱导的大鼠红细胞体内和体外氧化应激模型。我们确定了细胞形态，携氧能力，凋亡，抗氧化能力，和红细胞的能量代谢。还检查了Band3蛋白的酪氨酸磷酸化（pTyr）对RBC糖酵解的影响。
结果：GTS降低了最低浓度的H2O2诱导的红细胞溶血。此外，GTS有效地改善了形貌，增强了载氧能力，和增加抗氧化酶的活性，三磷酸腺苷（ATP）水平，和红细胞中的腺苷三磷酸酶（ATPase）活性。GTS还促进RBC中膜蛋白的表达，抑制Band3蛋白的pTyr，进一步改善糖酵解，恢复红细胞的形态结构和生理功能。
结论：这项研究表明，GTS可以通过改善红细胞形态和生理功能来保护红细胞免受氧化应激损伤。GTS处理前后pTyr表达及其相关pTyr调节酶的变化提示Band3蛋白是GTS治疗内源性和外源性氧化应激的主要靶点。此外，GTS可以通过抑制Band3蛋白的pTyr来增强红细胞的糖酵解能力，从而恢复红细胞的功能。
