摘要: | 低劑量阿斯匹靈 (aspirin) 被廣泛使用於心血管的保護,長期服用卻會增加消化性潰瘍之風險,現今雖有治療潰瘍的藥物但仍具有副作用。藻藍素為藍綠藻 (Spirulina platensis) 的有色蛋白,具有抗氧化與抗發炎的特性。寧夏枸杞 (Lycium barbarum L.) 是傳統草藥之一,枸杞多醣具有抗氧化劑與調節免疫之作用。本次實驗探討藻藍素與枸杞多醣對於阿斯匹靈誘導大鼠胃黏膜細胞 (RGM-1 cells) 發炎與凋亡之影響,細胞分別介入100、250及500 μg/mL的藻藍素與/或枸杞多醣24小時,再以21 mM的阿斯匹靈誘導損傷3小時。結果顯示阿斯匹靈會顯著降低細胞存活率,並顯著增加腫瘤壞死因子-α (tumor necrosis factor-α, TNF-α)、介白素-6 (interleukin-6, IL-6) 濃度、核轉錄因子-κB (nuclear factor-κB, NF-κB)、細胞外訊號調控激酶 (extracellular signal–regulated kinase, ERK)、p38、c-Jun胺基末端激酶 (c-Jun N-terminal kinase, JNK) 路徑的活化、Bax蛋白質表現量及caspase 3活性,並降低介白素-10 (interleukin 10, IL-10) 濃度,而介入藻藍素與/或枸杞多醣可以降低促發炎激素濃度、NF-κB、ERK、JNK路徑的活化、Bax蛋白質表現量及caspase 3活性,且增加抗發炎激素,顯示藻藍素與枸杞多醣可能藉由降低ERK的活化,進而降低發炎反應而達到抗發炎之作用,且枸杞多醣可能透過降低JNK的活化而減少阿斯匹靈誘導之細胞凋亡。 Aspirin is widely used for cardio-protection, and causes gastrotoxicity by impairing the epithelial defense through cyclooxygenase inhibition. C-phycocyanin (CPC) is a biliprotein pigment of the blue-green alga Spirulina platensis, and possesses antioxidant and anti-inflammatory properties. Lycium barbarum polysaccharides (LBP) extracted from wolfberry act as an antioxidant and immunomodulator. This study investigated the effects of CPC and LBP on aspirin-induced gastric damage in rat gastric mucosal RGM-1 cells. RGM-1 cells were pretreated with different concentrations of CPC and/or LBP (100, 250, and 500 μg/mL) for 24 hours, and gastric damage was induced by 21 mM aspirin for 3 hours. The results showed that aspirin significantly decreased cell viability of RGM-1 cells, interleukin 10 (IL-10), increased the pro-inflammatory markers, caspase 3 activity and Bax protein. Aspirin also increased nuclear factor-κB (NF-κB), extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 activation, while CPC and/or LBP increased IL-10, decreased pro-inflammatory markers, Bax protein, NF-κB, ERK and JNK activation. These results indicated that CPC and/or LBP could exert an anti-inflammatory effect on aspirin-induced gastric epithelial damage in RGM-1 cells by suppressing the activation of ERK signaling pathway and LBP may decrease apoptosis by suppressing the activation of JNK signaling pathway. |