人參總皂苷和小檗堿對肺癌PG細(xì)胞分泌免疫抑制性細(xì)胞因子的影響 醫(yī)學(xué)論文

1、    人參總皂苷和小檗堿對肺癌PG細(xì)胞分泌免疫抑制性細(xì)胞因子的影響 醫(yī)學(xué)論文              本文由中國論文范文收集整理。                         作者：郝鈺, 王萍, 吳珺

2、, 邱全瑛【摘要】   目的：觀察人參總皂苷（ginsenoside, Gs）和小檗堿（berberine, Ber）對腫瘤細(xì)胞分泌免疫抑制性細(xì)胞因子轉(zhuǎn)化生長因子1（transforming growth factor?beta1，TGF?1）和前列腺素E2（prostaglandin E2，PGE2）的影響，探討Gs和Ber對腫瘤免疫逃逸的作用機制。方法：首先建立人肺癌PG細(xì)胞與人T淋巴細(xì)胞株Jurkat細(xì)胞的共培養(yǎng)體系，隨機分為Gs（100 g/ml）組、Ber（10 g/ml）組、空白對照組和Jurkat組。用Gs和Ber作用PG細(xì)胞24 h后與Jurkat細(xì)胞共培養(yǎng)，24 h

3、后倒置顯微鏡下觀察Jurkat細(xì)胞生長的狀態(tài)；臺盼藍(lán)拒染實驗計數(shù)共培養(yǎng)6 h和24 h后Jurkat活細(xì)胞數(shù)；流式細(xì)胞儀檢測共培養(yǎng)24 h后Jurkat細(xì)胞的凋亡率；100、50、25 g/ml的Gs和10、5、2.5 g/ml的Ber分別處理PG細(xì)胞，并設(shè)空白對照組（PG細(xì)胞未經(jīng)藥物處理），酶聯(lián)免疫吸附測定法和放射免疫法檢測PG細(xì)胞上清液TGF?1和PGE2的含量。結(jié)果：Jurkat細(xì)胞與Gs和Ber處理過的PG細(xì)胞共培養(yǎng)后，其數(shù)目較空白對照組明顯減少，而凋亡率較空白對照組明顯增加；Gs和Ber可以增加PG細(xì)胞TGF?1的分泌，對PGE2的分泌無影響。結(jié)論：Gs和Ber可以增強PG細(xì)胞導(dǎo)致的

4、Jurkat細(xì)胞生長抑制和凋亡，其機制可能與Gs和Ber增加PG細(xì)胞分泌TGF?1有關(guān)。 【關(guān)鍵詞】   人參皂苷類; 小檗堿; 抑制因子, 免疫; 轉(zhuǎn)化生長因子1; 前列腺素E類Objective: To observe the effects of ginsenoside (Gs) and berberine (Ber), two kinds of active components of traditional Chinese herbal medicine, on transforming growth factor?beta1 (TGF?1) and prostagland

5、in E2 (PGE2) in PG cells.Methods: Co?culture system of human lung carcinoma cell line PG and human T lymphocyte cell line Jurkat was established. PG cells were treated with Gs (100 g/ml) and Ber (10 g/ml) for twenty?four hours, and then cocultured with Jurkat cells. After 24?hour coculture, the stat

6、e of Jurkat cells was observed with inverted microscope. The viable count of Jurkat cells was detected by trypan blue staining after 6? and 24?hour coculture, and the apoptosis of Jurkat cells was evaluated by flow cytometry. PG cells were treated with 100, 50, 25 g/ml Gs and 10, 5, 2.5 g/ml Ber res

7、pectively, and the content of TGF?1 and PGE2 in PG cells was detected by enzyme?linked immunosorbent assay (ELISA) and radioimmunoassay (RIA) method.Results: After coculture with PG cells treated with Gs and Ber, the number of Jurkat cells was less than blank control group, and the apoptosis rates o

8、f Jurkat cells in Gs? and Ber?treated groups were higher than blank control group. Gs and Ber could promote the secretion of TGF?1 in PG cells, but could not change the level of PGE2.Conclusion: Gs and Ber can promote the growth inhibition and apoptosis of Jurkat cells induced by PG cells, which may

9、 be related to the up?regulation of Gs and Ber on TGF?1 secretion in PG cells.Keywords: ginsenosides; berberine; suppressor factors, immunologic; transforming growth factor 1; prostaglandins E腫瘤的免疫逃逸機制復(fù)雜，可以通過自身分子表達(dá)的改變，如腫瘤特異性抗原的缺失、主要組織相容性抗原復(fù)合物（major histocompability complex, MHC）I類分子的缺乏、共刺激分子B7的缺陷、Fa

10、s分子下調(diào)耐受凋亡以及“Fas反擊”和分泌免疫抑制性細(xì)胞因子等，使腫瘤不能有效地被免疫細(xì)胞識別和攻擊，甚至主動下調(diào)宿主免疫功能，從而逃避抗腫瘤免疫反應(yīng)。我們的前期研究結(jié)果表明，Jurkat細(xì)胞與PG細(xì)胞共培養(yǎng)后數(shù)目減少，人參總皂苷（ginsenoside, Gs）和小檗堿（berberine, Ber）可以促進(jìn)PG細(xì)胞的這種作用，該結(jié)果可能與Gs和Ber增加PG細(xì)胞的FasL表達(dá)，促進(jìn)PG細(xì)胞誘導(dǎo)Jurkat細(xì)胞凋亡的“Fas反擊”作用有關(guān)。但Jurkat細(xì)胞與PG細(xì)胞共培養(yǎng)后數(shù)目減少的原因除與“Fas反擊”誘導(dǎo)的凋亡有關(guān)外，也有可能與PG細(xì)胞分泌某些免疫抑制性細(xì)胞因子相關(guān)。本研究檢測了PG細(xì)

11、胞分泌轉(zhuǎn)化生長因子1（transforming growth factor?beta1，TGF?1）和前列腺素E2（prostaglandin E2, PGE2）的情況以及Gs和Ber對此的影響。1  材料與方法 1.1  細(xì)胞株  人高轉(zhuǎn)移性肺癌細(xì)胞PG（本室保存）；人T淋巴細(xì)胞株Jurkat（ 中國 醫(yī)學(xué) 科學(xué) 院基礎(chǔ)醫(yī)學(xué)研究所）。1.2  藥物與主要試劑  Gs（北京天然藥物研究院趙銳博士惠贈）；Ber（中國藥品生物制品檢定所）；Annexin?V FITC細(xì)胞凋亡檢測試劑盒（北京寶賽生物技術(shù)有限公司）；人TGF?1檢測試劑盒（武漢博士德生物工程有限公司）；人PGE2放射免疫分析試劑盒（蘇州大學(xué)血液學(xué)研究所）。 關(guān)鍵詞:抑制,影響,免疫,細(xì)胞,人參,醫(yī)學(xué)論文,人參總皂苷和小檗堿對肺癌PG細(xì)胞分泌免疫抑制性細(xì)胞因子的影響 內(nèi)容摘要:本文