腦癌目前在醫學上的治療方法，仍然是極度缺乏的，而神經膠質瘤又是腦癌分類中最惡性的一種。過去有許多從天然物中尋找抗癌藥物的例子，例如紫杉醇、長春花鹼等等。Lauryl gallate (LG) 是一種廣泛存在於植物中的抗氧化成分，而許多文獻也曾報導在許多人類癌細胞中具有抗癌的活性，但是尚未被證實於人類的腦癌細胞中，因此本研究著重於利用人類神經膠質瘤細胞U87及小鼠神經膠質瘤細胞ALTS1C1當作抗癌活性的驗證平台。
在使用LG處理腦癌細胞實驗的過程中，我們觀察藥物處理前後癌細胞的型態和存活率的改變，以及Annexin V/PI雙染的實驗，來評估細胞凋亡的程度。在人類腦癌U87細胞中，發現LG處理後的細胞凋亡路徑是藉由caspase dependent的訊息傳遞路徑所造成；並且也使用西方墨點法來驗證LG可以誘發許多與細胞凋亡相關的蛋白質表現。而在體外細胞遷移的實驗中，也觀察到LG可以抑制U87人類腦癌細胞的轉移，同時在小鼠神經膠質瘤的實驗中也證實，LG造成ALTS1C1小鼠腦癌細胞的細胞凋亡，並且降低細胞的轉移；在活體癌症動物模型中，LG可以延緩小鼠腫瘤的生長。而在免疫螢光染色的切片中，也發現使用LG的小鼠腫瘤切片，HIF-2α和腫瘤缺氧(PIMO)的表現也是下降的。動物心臟超音波測量也證實小鼠在LG處理下不會影響左心室收縮和舒張的距離，即為左心室的縮短分率沒有改變，也就是證實LG在小鼠癌症模型中，連續投予80 mg/kg的LG並不會有心臟毒性的產生。
因此，我們在以上實驗結果發現LG可以造成U87和ALTS1C1細胞的型態改變，並且降低其存活率，是藉由細胞凋亡及caspase的路徑。另外，LG也會調控細胞中的缺氧因子蛋白的表現。本篇研究在人類及小鼠神經膠質瘤的實驗上證實LG在細胞上及小鼠動物實驗中具有抗腦癌的療效。

Glioblastoma is the most frequent glioma, consisting of 65% glioma. However, treatment of human glioma tumor is still an unmet medical need. Natural products are always promising resources for discovery of anticancer drugs. Lauryl gallate (LG) is one of the derivatives of gallic acid, widely present in plants, and has been shown to induce anticancer activities in many human cancer cell lines; however, it has not been studied in human glioma cell lines. Thus, the effects of LG on human glioblastoma ,U87 cells, and mouse astrocytoma, ALTS1C1 cells, were investigated in the present in-vitro and in-vivo. Cell morphology and viability were examined by phase-contrast microscopy. Annexin V/Propidium iodide (PI) double staining were performed and assayed by flow cytometry to investigate whether LG-induced cell death was due to the induction of apoptosis. Furthermore, LG-treated U87 cells were analyzed by caspase activity assay at various concentrations. To further demonstrate the mechanism of LG-induced apoptotic cell death, the expression of apoptosis-associated proteins were examined in U87 and ALTS1C1 cells after LG treatment by western blot. In this study, LG-induced morphological changes and decreased cell viability in U87 and ALTS1C1 cells were demonstrated. Annexin V/PI double staining exhibited that LG induced apoptosis in U87 and ALTS1C1 cells in a dose-dependent manner. The increased activities of caspase-2, -3, -8 and -9 demonstrated that LG induced apoptosis of U87 cells through a caspase-dependent pathway. In terms of molecular level, LG increased pro-apoptotic proteins (Bax and Bak) and decreased anti-apoptotic protein (Bcl-2) in U87 and ALTS1C1 cells. Moreover, LG also showed tumor growth delay in a mouse ALTS1C1 allograft tumor model. We also examined the heart fraction shorting (FS) to evaluate the drug cardiotoxicity by mouse echocardiography. The results showed that LG had no cardiotoxicity in the allograft brain tumor model because there were no significant changes of the heart left ventricular (LV) diameter.

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