s-allyl cysteine（SAC）、s-propyl cysteine（SPC）是來自大蒜的水溶性含硫化合物之衍生物，本實驗室過去的研究已經證實這兩種含硫化合物有抗氧化保護的作用。因此更進一步探討，Balb/cA老鼠飲水中添加兩種含硫化合物（1 g/L）四週，對於預防acetaminophen（350 mg/kg）誘發肝臟傷害的保護效果。結果發現acetaminophen誘發肝毒性的小鼠血清中天門冬氨酸轉胺（AST）和丙氨酸轉胺（ALT）顯著上升，麩胱（GSH）大量損耗，麩胱過氧化（GPX）和過氧化氫（catalase）活性降低，脂質過氧化程度增加，顯示氧化壓力增加（p<0.05）。同時C反應蛋白（CRP）、von Willebrand factor（vWF）、腫瘤壞死因子（TNF-α）、IL-6和IL-10皆顯著上升（p<0.05）。然而，在小鼠飲水添加SAC和SPC後再以acetaminophen誘發肝毒性，不僅減緩GSH消耗，及ALT、AST下降，也降低氧化傷害的程度，更顯著抑制acetaminophen所引起CRP、vWF、TNF-α、IL-6和IL-10的增加（p<0.05）。在凝血與纖溶系統方面，誘發acetaminophen之後，纖維蛋白溶解原活化抑制劑-1（plasminogen activator inhibitor-1）活性和纖維蛋白原顯著增加（p<0.05），蛋白C（protein C）和抗凝血素Ⅲ（antithrombin-Ⅲ；AT-Ⅲ）則顯著降低（p<0.05）。然而飲水中添加SAC和SPC，顯著改善acetaminophen引起的protein C和AT-Ⅲ下降（p<0.05）。所有結果顯示SAC和SPC這兩種大蒜的水溶性含硫化合物，對肝臟具有多重保護的效果。
In vivo protective effects of s-allyl cysteine (SAC) and s-propyl cysteine (SPC) against acetaminophen-induced hepatotoxicity in Balb/cA mice were studied. SAC and SPC at 1 g/L were added into drinking water for four weeks and followed by acetaminophen treatment. Acetaminophen treatment significantly depleted glutathione content, increased oxidation stress and elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities (P < 0.05); however, the intake of SAC or SPC significantly alleviated glutathione depletion and the elevation of ALT and AST, enhanced glutathione peroxidase activity, and lowered malondialdehyde formation (P < 0.05). Plasma levels of C-reactive protein (CRP), von Willebrand factor (vWF), IL-6, IL-10 and TNF-alpha were significantly increased by acetaminophen treatment (P < 0.05); and SAC or SPC intake significantly suppressed acetaminophen-induced elevation of CRP, vWF and the three cytokines (P < 0.05). Acetaminophen treatment also significantly increased plasminogen activator inhibitor-1 (PAI-1) activity and plasma fibrinogen level, and decreased antithrombin III (AT-III) and protein C activities (P < 0.05). SAC or SPC intake alleviated AT-III and protein C reduction (P < 0.05); but did not affect PAI-1 activity and plasma fibrinogen level (P > 0.05). These data suggest that SAC and SPC are potential multiple-protective agents against acetaminophen-induced hepatotoxicity.
