80年代土耳其译制电影,80年代外国电影|80年代外国电影有哪些_80年代外国经典电影在线播放地址是多少?

[1]陳康堯,顧恩毅,蔡碰德,等.H1受體拮抗劑異丙嗪對順鉑治療骨肉瘤的影響及機(jī)制[J].福建醫(yī)藥雜志,2021,43(04):132-136.
 CHEN Kangyao,GU Enyi,CAI Pengde,et al.Efficacy and mechanism of H1 receptor antagonist promethazine on osteosarcoma treated with cisplatin[J].FUJIAN MEDICAL JOURNAL,2021,43(04):132-136.
點(diǎn)擊復(fù)制

H1受體拮抗劑異丙嗪對順鉑治療骨肉瘤的影響及機(jī)制()
分享到:

《福建醫(yī)藥雜志》[ISSN:1002-2600/CN:35-1071/R]

卷:
43
期數(shù):
2021年04期
頁碼:
132-136
欄目:
基礎(chǔ)研究
出版日期:
2021-08-15

文章信息/Info

Title:
Efficacy and mechanism of H1 receptor antagonist promethazine on osteosarcoma treated with cisplatin
文章編號(hào):
1002-2600(2021)04-0132-05
作者:
陳康堯顧恩毅蔡碰德潘偉坤鄭忠
廈門大學(xué)附屬福州第二醫(yī)院骨科(福州 350007)
Author(s):
CHEN KangyaoGU EnyiCAI PengdePAN WeikunZHENG Zhong
Department of Orthopedics, Fuzhou Second Hospital Affiliated To Xiamen University, Fuzhou, Fujian350007,China
關(guān)鍵詞:
異丙嗪順鉑骨肉瘤化療抵抗地塞米松
Keywords:
promethazinecisplatinosteosarcomachemotherapy-resistancedexamethasone
分類號(hào):
R738.1
文獻(xiàn)標(biāo)志碼:
B
摘要:
目的 觀察異丙嗪在骨肉瘤細(xì)胞對順鉑化療敏感性的影響,探討其用于替代地塞米松(Dex)作為化療輔助藥物的可行性。 方法 構(gòu)建荷人骨肉瘤裸鼠模型,隨機(jī)分成6組,每組6只。分別腹腔注射200 μL的生理鹽水、化療藥物順鉑(3 mg/kg)、Dex(4 mg/kg)、異丙嗪(20 mg/kg)、Dex+順鉑、異丙嗪+順鉑治療。每隔3天給藥1次,共4次。定期測量腫瘤體積大小,至第15天麻醉處死小鼠取腫瘤組織,稱量瘤體重量。免疫熒光染色法檢測腫瘤組織中血管內(nèi)皮細(xì)胞標(biāo)志物CD31的表達(dá)和分布;觀察上述不同藥物處理對骨肉瘤細(xì)胞株MG-63細(xì)胞血管內(nèi)皮細(xì)胞生長因子VEGF表達(dá)和分泌的影響;MTT法檢測MG63的增殖及順鉑誘導(dǎo)的增殖抑制作用;用Annexin V-FITC/PI雙染法檢測異丙嗪和順鉑對MG-63細(xì)胞凋亡的影響。 結(jié)果 與單用順鉑治療組相比,異丙嗪+順鉑組與Dex+順鉑組的腫瘤體積和離體瘤重均顯著增大。Dex+順鉑組和異丙嗪+順鉑組腫瘤間質(zhì)組織中CD31的表達(dá)和分布明顯多于單用順鉑組。單用Dex或異丙嗪處理24 h或36 h并不改變VEGF mRNA和蛋白分泌水平,單用順鉑處理則可明顯降低VEGF的表達(dá)和分泌,而異丙嗪與順鉑聯(lián)用則可顯著逆轉(zhuǎn)順鉑的作用。10 nM~10 μM異丙嗪處理MG63細(xì)胞72 h,僅10 nM異丙嗪對細(xì)胞增殖抑制作用,抑制率約為25.7%;與 2 μg/mL順鉑聯(lián)用時(shí),異丙嗪也不能逆轉(zhuǎn)順鉑對細(xì)胞增殖抑制作用。聯(lián)用Dex可以部分逆轉(zhuǎn)順鉑導(dǎo)致的細(xì)胞凋亡,凋亡率為12.7%,而聯(lián)用異丙嗪并不能減少順鉑對細(xì)胞的凋亡誘導(dǎo)作用。 結(jié)論 骨肉瘤化療時(shí)使用H1受體拮抗劑異丙嗪會(huì)降低化療藥的效果,機(jī)制可能與異丙嗪促進(jìn)腫瘤血管生成有關(guān)。
Abstract:
Objective To observe the effect of promethazine on the sensitivity of cisplatin chemotherapy in osteosarcoma cells,and to explore the feasibility of using it as a substitute for dexamethasone (Dex) as an adjuvant chemotherapy.Methods A nude mouse model bearing human osteosarcoma was constructed and randomly divided into 6 groups with 6 mice in each group.Inject 200 μL of normal saline, chemotherapy drugs cisplatin (3 mg/kg), Dex (4 mg/kg), promethazine(20 mg/kg),Dex+cisplatin,promethazine+cisplatin respectively.It was administered once every 3 days for a total of 4 times.The tumor volume was measured regularly,until the 15th day the mice were anesthetized and the tumor tissues were taken and the tumor weight was weighed.lmmunofluorescence staining method was used to detect the expression and distribution of vascular endothelial cell marker CD31 in tumor tissues.The effects of the above-mentioned different drug treatments on the expression and secretion of vascular endothelial growth factor VEGF in MG-63 cells were observed.MTT method was used to detect osteosarcoma cell line MG63 Proliferation and cisplatin-induced proliferation inhibition.Annexin V-FITC/PI double staining method was used to detect the effect of promethazine and cisplatin on the apoptosis of MG-63 cells.Results Compared with the cisplatin treatment group alone, the tumor volume and isolated tumor weight of the promethazine+cisplatin group and the Dex+cisplatin group were significantly increased.The expression and distribution of CD31 in tumor interstitial tissues of Dex+cisplatin group and promethazine+cisplatin group were significantly higher than that of cisplatin alone group.Treatment with Dex or promethazine alone for 24 hours or 36 hours does not change the levels of VEGF mRNA and protein secretion.Treatment with cisplatin alone can significantly reduce the expression and secretion of VEGF,while the combination of promethazine and cisplatin can significantly reverse cisplatin.The role of platinum.When MG63 cells were treated with 10nM-10μM promethazine for 72 hours, only 10 nM promethazine inhibited cell proliferation, and the inhibition rate was about 25.7%; when combined with 2 μg/mL cisplatin, promethazine could not reverse the inhibition of cisplatin on cell proliferation.effect.Combined use of Dex can partially reverse the apoptosis caused by cisplatin,with an apoptotic rate of 12.7%,while combined use of promethazine cannot reduce the apoptosis-inducing effect of cisplatin on cells.Conclusion The use of H1 receptor antagonist promethazine during chemotherapy of osteosarcoma may reduce the effect of chemotherapy drugs, and the mechanism may be related to the promotion of tumor angiogenesis by promethazine.

參考文獻(xiàn)/References:

[1]Reed D R,Hayashi M,Wagner L,et al.Treatment pathway of bone sarcoma in children,adolescents,and young adults[J].Cancer,2017,123(12):2206-2218.
[2]Roberts R D,Lizardo M M,Reed D R,et al.Provocative questions in osteosarcoma basic and translational biology:a report from the children's oncology group[J].Cancer,2019,125(20):3514-3525.
[3]Herr I,Büchler M W,Mattern J.Glucocorticoid-mediated apoptosis resistance of solid tumors[J].Results Probl Cell Differ,2009(49):191-218.
[4]Gassler N,Zhang C,Wenger T,et al.Dexamethasone-induced cisplatin and gemcitabine resistance in lung carcinoma samples treated ex vivo[J].Br J Cancer,2005,92(6):1084-1088.
[5]Zhang C,Kolb A,Mattern J,et al.Dexamethasone desensitizes hepatocellular and colorectal tumours toward cytotoxic therapy[J].Cancer Lett,2006,242(1):104-110.
[6]Diao F,Chen K,Wang Y,et al.Involvement of small G protein RhoB in the regulation of proliferation,adhesion and migration by dexamethasone in osteoblastic cells[J].PLoS One,2017,12(3):e0174273.
[7]中國抗癌協(xié)會(huì)癌癥康復(fù)與姑息治療專業(yè)委員會(huì),2中國臨床腫瘤學(xué)會(huì)抗腫瘤藥物安全管理專家委員會(huì).腫瘤治療相關(guān)嘔吐防治指南(2014版)[J].臨床腫瘤學(xué)雜志,2014,19(3):263-273.
[8]Kars M D,Iseri O D,Gunduz U,et al.Reversal of multidrug resistance by synthetic and natural compounds in drug-resistant MCF-7 cell lines[J].Chemotherapy,2008,54(3):194-200.
[9]Donmez,Yaprak et al.Effect of MDR modulators verapamil and promethazine on gene expression levels of MDR1 and MRP1 in doxorubicin-resistant MCF-7 cells[J].Cancer Chemotherapy and Pharmacology,2011,67(4):823-828.
[10]Gajdács,Márió et al.Phenothiazines and Selenocompounds:A Potential Novel Combination Therapy of Multidrug Resistant Cancer[J].Anticancer Research,2020,40(9):4921-4928.

備注/Memo

備注/Memo:
基金項(xiàng)目:福州市衛(wèi)生計(jì)生中青年科學(xué)研究項(xiàng)目 (2018-S-wq12)
更新日期/Last Update: 2021-08-15