目的 研究云樹果實醋酸乙酯提取物（EGCF）對H22實體移植瘤的抑制活性及作用機制。方法 皮下接種H22瘤株建立小鼠H22實體移植瘤模型，隨機分為模型組、環(huán)磷酰胺（20 mg/kg，陽性對照，ip給藥）組和EGCF高、中、低劑量（400、200、100 mg/kg，ig給藥）組，連續(xù)給藥10 d，另設(shè)一對照組。檢測小鼠體質(zhì)量變化、抑瘤率及脾臟指數(shù)，ELISA法測定血清中白細胞介素-6（IL-6）、腫瘤壞死因子-α（TNF-α）、轉(zhuǎn)化生長因子-β1（TGF-β1）的含量，HE染色法觀察腫瘤組織病理學(xué)改變，免疫組化法檢測腫瘤組織p-STAT3及血管內(nèi)皮生長因子（VEGF）的表達。結(jié)果 與模型組比較，EGCF高、中、低劑量組小鼠的腫瘤質(zhì)量均顯著降低（P<0.01、0.001），脾臟指數(shù)均無顯著性差異；高、低劑量組小鼠血清中IL-6水平顯著降低（P<0.05），各劑量組TNF-α含量顯著增加（P<0.05、0.01）；各劑量組瘤組織均出現(xiàn)較多紅染、碎片狀的干酪樣壞死區(qū)域，且伴有大量空泡形成；各劑量組均顯著減少腫瘤組織VEGF表達，高劑量組顯著抑制STAT3磷酸化（P<0.05、0.01）。結(jié)論 EGCF能夠抑制H22實體移植瘤生長，其機制可能與阻斷STAT3相關(guān)信號通路有關(guān)。

Objective To investigate the anti-tumor effect and mechanism of EtOAC extract from Garcinia cowa fruits (EGCF) on H22-bearing mice. Methods Subcutaneous inject H22 cells into mouse to establish H22 tumor model, then randomly divided into model group, CTX (20 mg/kg, positive control) group and EGCF high, medium and low dose (400, 200 and 100 mg/kg) groups. Continuous infusion for 10 d, and set an extra control group then measure the body weight changing, anti-tumor rate and sleepen index of each mice. ELISA assay was used to measure IL-6, TNF-α and TGF-β1 in serum. Pathologic changes of tumor tissue were be observed by HE staining. The expressions of p-STAT3 and VEGF were tested by IHC assay. Results Compared with model group, the tumor quality of the mice in the EGCF high, middle and low dose groups of EGCF decreased significantly (P<0.01 and 0.001), and there was no significant difference in the spleen index. The level of IL-6 in the serum of high and low dose groups was significantly decreased (P<0.05), and the content of TNF-α in each dose group increased significantly (P<0.05, 0.01). A large number of red stained and fragmented caseous necrosis area and a large number of vacuoles were found, and the VEGF expression of tumor tissue was significantly reduced in each dose group. The high dose group significantly inhibited the phosphorylation of STAT3 (P<0.05 and 0.01). Conclusion EGCF could inhibit the growth of H22 tumor cells, and the mechanism may be relevant to block STAT3 related cell signaling.

國家自然科學(xué)基金資助項目（31370379）；國家重大新藥創(chuàng)制科技重大專項（2017Z09301060）