黃芩苷 (Baicalin) 是黃酮類的一種，具有抗氧化、抗病毒及抗癌與其他生理活性。本研究目的為：(1) 探討黃芩苷對 C2C12 小鼠骨骼肌細胞之抗糖尿病效應之影響；(2) 檢測黃芩苷對棕櫚酸 (palmitic acid, PA) 誘導細胞之抗發炎活性之影響。結果顯示，黃芩苷在所有濃度均具有保護細胞的效力。從 25 μM 到 50 μM的黃芩苷可顯著的升調節葡萄糖的吸收效率。在西方墨點法分析結果發現黃芩苷可有效率的升調節 PI3K、p-Akt、p-IRS-1 及 GLUT4 之蛋白表現，對 p-ERK 的表現有些微的提高，並不影響 Akt、p38、p-38、JNK、p-JNK 及 ERK 的蛋白表現。黃芩苷對棕櫚酸-刺激細胞作用 24 小時之細胞存活率結果發現，細胞於棕櫚酸刺激後存活率降至 70% 而經由黃芩苷處理後可回升至 90%。黃芩苷對棕櫚酸-刺激細胞作用 6 小時，可有效的抑制 IL-6 及 IL-10 的表現，而對 TNF-α 的抑制效果較不明顯。由上述結果顯示黃芩苷在抗糖尿病及抗發炎的效應上扮演一個主要的角色，可能是透過葡萄糖吸收、胰島素的訊息路徑及抑制發炎的細胞激素之產生所致。 Baicalin is a flavonoid that possess antioxidant, anti-viral, anti-cancer and other physiological activities. The aims of this study were (1) to study the anti-diabetic effect of baicalin in the murine C2C12 skeletal muscle cells, and (2) to examine the anti-inflammatory activity of baicalin in palmitic acid (PA)-induced cells. The results from the study showed protection effects at all concentrations of baicalin tested. From 25 to 50 μM baicalin significantly up-regulated of the glucose absorption. The results from western blot revealed that baicalin effectively up-regulated the expression of PI3K, p-Akt, p-IRS-1 and GLUT4 proteins, with less obvious effect on p-ERK. Furthermore, baicalin did not affect the expression of Akt, p38, p-p38, JNK, p-JNK, and ERK proteins. Results on baicalin is effect on palmitic acid-stimulated cell function revealed that cell viability after palmitic acid stimulation reduced to 70% while baicalin protected the cells to 90%. Baicalin remarkly suppressed the expression of IL-6 and IL-10 in PA-stimulated cells. The inhibitory effect on TNF-α was not significant. These results suggest that baicalin may play a potentral role in the anti-diabetic and anti-inflammatory effects through glucose up-take, insulin signaling pathways, and inhibiting the production of inflammatory cytokines.
