山苦瓜 (Momordica charantia L. var. abbreviata Ser.) 屬一年生蔓性攀緣草本葫蘆科 (Cucurbitaceae) 植物,別名野苦瓜、短果苦瓜或小苦瓜,產期為4 至9 月,在傳統漢藥書籍中已記載明確功效。近來有科學研究發現苦瓜可以活化轉錄因子PPAR 進而調控其下游基因之表現,且已知PPARγ 的活化與抗糖尿病、抗發炎、抗病毒、抗癌等免疫調節有關。故本研究主要探討山苦瓜(包括莖、葉、花、渣)之乙酸乙酯萃取物與汁的水萃物對發炎反應及其相關基因、蛋白質之表現影響。以小鼠巨噬細胞株RAW264.7 為模式,並以山苦瓜不同部位之萃取物分別處理不同濃度(10、50、100 μg/mL)及LPS 100 ng/mL同時處理細胞。在MTT 實驗發現各山苦瓜萃取物並不會顯著促進細胞增生(P>0.05)。另外Transient transfection 實驗發現,山苦瓜渣(含籽)乙酸乙酯萃取物於100 μg/mL 時,具有顯著活化PPARγ 之能力(P <0.05)。而在發炎介質NO2、PGE2 方面,則以山苦瓜渣(含籽)乙酸乙酯萃取物於100 μg/mL 時之抑制效果最好(P<0.05)。綜合上述,山苦瓜渣乙酸乙酯萃取物具有活化PPARγ 的能力且可以降低COX-2 蛋白質表現及其抑制催化PGE2 之生成;NO2 生成亦被抑制。 此外,觀察到人類細胞激素如:IL-1 家族與IL-3 等基因的表現皆受到抑制。推測其可能機轉與PPARγ 的活化進而抑制NF-κB 的作用以及細胞激素互相競爭受器有關。
Wild bitter gourd (Cucurbitaceae) is an annual herbaceous vines climbing plant. It is also named wild balsam pear, short fruit bitter gourd or small bitter gourd, which crops from April to September. In traditional Chinese medical textbook, it already records definite efficacy for internally and externally application of wild bitter gourd. Recently, the scientific research showed that bitter gourd extracts could activate such as transcription factors PPAR (Peroxisome Proliferator-Activated Receptor). In the previous studies, activators of PPARγ may be potential in anti-diabetic, anti inflamanatory, anti-viral and anti-cancer related immunomodulation effects. Therefore, this study will focus on exploring the ethyl acetate extracts of wild bitter gourd(stem, leaf, flower and fruit) and juice of water soluble extracts on the inflammatory responses of related genes and proteins expression. Using different parts of wild bitter gourd extracts, respectively, RAW264.7 macrophage cells were treated with different concentrations (10、50、100 μg/mL)and LPS . The MTT assay results showed that wild bitter gourd extract treatments did not significantly influence the cell viability. Furthermore, transient transfection assay showed that extracts of wild bitter gourd residue at the concentration of 100 μg/mL activated PPARγ. Inflammatory mediators such as PGE2 and NO2 showed that extracts of wild bitter residue at 100 μg/mL had the potential in inhibitory ability against inflammation. These results in this study also indicated that extracts of wild bitter gourd IX residue activated PPARγ and suppressed the COX-2 protein expression. Furthermore, the human cytokine genes such as IL-1family and IL-3 expression were inhibition. Therefore, we suggest the possible mechanism is via activating the PPARγ signaling pathway and then suppress the NF-κB activation.