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[1]彭磊,程少文,沈躍,等.二氮嗪對軟骨細胞氧化損傷的影響[J].中醫(yī)正骨,2014,26(05):3-8.
　Peng Lei*,Cheng Saowen,Shen Yue,et al.Diazoxide influence on cartilage cells from oxidative damage[J].The Journal of Traditional Chinese Orthopedics and Traumatology,2014,26(05):3-8.
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二氮嗪對軟骨細胞氧化損傷的影響()
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《中醫(yī)正骨》[ISSN:1001-6015/CN:41-1162/R]

卷:
第26卷
期數:
2014年05期
頁碼:
3-8
欄目:
基礎研究
出版日期:
2014-05-31

文章信息/Info

Title:
Diazoxide influence on cartilage cells from oxidative damage
作者:
彭磊1; 程少文1; 沈躍2; 應曉洲2; 趙志蓉2; 安濤2; 周英勇2; 程曉杰2; 陳慶玉2; 呂傳柱3
1.海南醫(yī)學院附屬醫(yī)院,海南 海口 570100; 2.溫州醫(yī)科大學,浙江 溫州 325000; 3.海南醫(yī)學院,海南 海口 570100
Author(s):
Peng Lei*;  Cheng Saowen;  Shen Yue;  Ying Xiaozhou;  Zhao Zhirong;  An Tao;  Zhou Yingyong;  Cheng Xiaojie;  Chen Qingyu;  Lu Chuanzhu.*
The affiliated hospital to Hainan medical colledge, Haikou, 570100,Hainan,China
關鍵詞:
二氮嗪 軟骨細胞 活性氧 凋亡
Keywords:
Diazoxide;  Chondrocytes;  Reactive oxygen species;  Apoptosis
摘要:
目的:探討二氮嗪對雙氧水誘導的軟骨細胞氧化損傷的影響。方法:取SD乳鼠膝關節(jié)軟骨細胞進行原代培養(yǎng),將對數生長期的軟骨細胞分成5組,分別為陰性對照組(A組),雙氧水組(B組),H2O2+0.1 μmol·L-1二氮嗪組(C組),H2O2+1.0 μmol·L-1二氮嗪組(D組),H2O2+10 μmol·L-1二氮嗪組(E組); A組細胞不做特殊處理,B組用0.3 mmol·L-1雙氧水在37 ℃恒溫箱內孵育4 h,C、D、E、F組預先分別用0.1 μmol·L-1 DZ, 1.0 μmol·L-1DZ,10 μmol·L-1DZ,100 μmol·L-1在37℃的恒溫箱孵育30分鐘,PBS洗滌細胞,再用0.3 mmol·L-1雙氧水在37℃恒溫箱內孵育4小時。分別檢測ABCDE各組細胞的細胞活性,ROS的量,細胞凋亡情況。結果:①MTT法檢測各組細胞活性,細胞活性率從大至小依次為D組>C組>E組>F組>B組; ②用活性氧探針DCFH-DA檢測各組細胞中的ROS的量,ROS產量從多至少依次為B組>E組>D組>C組>A組; ③流式細胞儀檢測各組細胞凋亡情況,各組細胞凋亡率由大至小依次為B組>E組>D組>C組。④Western bolt檢測各組軟骨細胞中HIF-1α蛋白的表達,各組軟骨細胞中HIF-1α蛋白表達量依次為C組>D組>E組>A組>B組。結論:二氮嗪可降低雙氧水誘導的軟骨細胞的凋亡率,同時也降低雙氧水誘導的軟骨細胞ROS的產生,并誘導軟骨細胞產生HIF-1α蛋白,可能存在二氮嗪誘導HIF-1α的表達,引起下游相關基因的轉錄,總體提高軟骨細胞對氧化損傷的耐受力,阻礙自由基誘導的軟骨細胞的凋亡。
Abstract:
Objective:To investigate diazoxide infection in hydrogen peroxide induced cartilage cells.Method:We obtain the carilage cells from the SD neonatal rat articular cartilages. The cartilage cells were divided into five groups,namely the control group(A), the hydrogen peroxide group(B),H2O2 + 0.1 μmol·L-1DZ group(C), H2O2 +1.0 μmol·L-1 DZ group(D), H2O2 +10 μmol·L-1 DZ group(E); group A had no special treatment,group B incubated with 0.3 mmol/L hydrogen peroxide for 4 hours in 37 ℃ incubator, the C, D, E group were preincubated with 0.1 μmol·L-1DZ 1.0 μmol·L-1DZ,10 μmol·L-1 DZ in a 37 ℃ incubator incubated 30 minutes, then incubated with 0.3 mmol·L-1 hydrogen peroxide solution in 37 ℃ incubator.The amount of the ROS and the apoptosis rate of cells in each group were detected.Results:①.Using the MTT assay, the order of the rate of cells activity: group A> group D > group C > group E >group B. ②. The ROS productions were detected by the DCFH-DA, the order of ROS production as follow: group B> group E> group D> group C> group A. ③. The apoptosis rates of cells were detected by Flow cytometer.The order of apoptosis rates of cartilage cells as follow: group B> group E> group D> group C group.④. the expression of HIF-1α in each chondrocytes group detected by western blot,as follow: group C> group D > group E > group A > group B.Conclusion:Diazoxide can reduce the apoptosis rates of hydrogen peroxide-induced chondrocytes, while also reducing the ROS production of the hydrogen peroxide-induced chondrocyte.It can be inferred that,diazoxide may reduce the apoptosis rates and mortality of chondrocyte by reducing the ROS production of chondrocyte and increasing the expression of HIF-1α protein.

參考文獻/References:

[1] Sutipornpalangkul W,Morales NP,Harnroongroj T.Free radicals in primary knee osteoarthritis[J].J Med Assoc Thai,2009,92(6):268-274.
[2] Grishko VI,Ho R,Wilson GL,et al.Diminished mitochondrial DNA integrity and repair capacity in OA chondrocytes[J].Osteoarthritis Cartilage,2009,17(1):107 -113.
[3] Minners J,Locerdal,Yellon OM,et al.Diazoxide-induced respiratory inhibition—a putative mitochondrial K ATP channel independent mechanism of pharmacological preconditioning[J].Mol and Cell Biochemistry,2007,294(9):11.
[4] McCully JD,Wakiyama H,Cowan DB,et al.Diazoxide amelioration of myocardial injury and mitochondrial damage during cardiac surgery[J].Ann Thorac Surg,2002,74(7),2138-2145.
[5] Shane Anderson A,Loeser RF.Why is osteoarthritis an age-related disease[J].Best Pract Res Clin Rheumatol,2010,24(8):15-26.
[6] Xie J,Duan L,Qian X,et al.K-ATP Channel Openers Protect Mesencephalic Neurons Against MPP+-Induced Cytotoxicity Via Inhibition of ROS Production[J].J Neurosci.2010,88(2):428-437.
[7] Virgili N,Espinosa-Parrilla JF,Mancera P,et al.Oral administration of the KATP channel opener diazoxide ameliorates disease progression in a murine model of multiple sclerosis[J].J Neuroinflammation,2011,8(2):149.
[8] Kukreja RC.Mechanism of reactive oxygen species generation after opening of mitochondrial KATP channels[J]. Am J Physiol Heart Circ Physiol,2006,291(5):2041-2043.
[9] Shao SX,Zhang L,Chen HX,et al.Diazoxide pretreatment enhances L6 skeletal myoblast survival and inhibits apoptosis induced by hydrogen peroxide[J].Anat Rec(Hoboken),2012,295(4):632-640.
[10] Choi EM,Kim GH,Lee YS.Diazoxide protects against hydrogen peroxide-induced toxicity in the osteoblastic MC3T3-E1 cells[J]. Eur J Pharmacol,2009,624(1-3):45-50.
[11] Zhang H,Zhao D,Wang Z,et al.Diazoxide preconditioning alleviates caspase-dependent and caspase-independent apoptosis induced by anoxia-reoxygenation of PC12 cells[J].J Biochem,2010,148(4):413-421.
[12] Patel NS,Muneer A,Blick C,et al.Targeting vascular endothelial growth factor in renal cell carcinoma[J].Tumour Biol,2009,30(6):292-299.

更新日期/Last Update: 1900-01-01