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NMT是基因功能的活體檢測技術(shù)，已被103位諾貝爾獎得主所在單位，及北大、清華、中科院使用。

期刊：Bone

主題：DAla2GIP抑制鈣吸收拮抗軟骨細胞凋亡

標(biāo)題：DAla2GIP antagonizes H2O2-induced chondrocyte apoptosis and inflammatory factor secretion

影響因子：4.360

檢測指標(biāo)：Ca2+流速

檢測樣品：7日齡小鼠，1.0ml乙麻醉后處死，第三代胸部軟骨組織細胞

Ca2+流實驗處理方法：

Control，300μM H2O2 ，100pM DAla2GIP 和 300μM H2O2+ 100pM DAla2GIP

Ca2+流實驗測試液成份：無

作者：山西醫(yī)科大學(xué)第二醫(yī)院衛(wèi)小春、王宇澤

英文摘要

To investigate the protective effects of DAla2GIP against the apoptosis and inflammatory factor secretion in H2O2-induced chondrocyte, and explore the possible mechanisms of DAla2GIP underlying its protection.

The chondrocytes were divided into the following four groups: Control, 300?μM H2O2, 100?pM DAla2GIP and 300?μM H2O2?+?100?pM DAla2GIP. The apoptosis of chondrocyte was measured by using mitochondrial membrane potential assay kit (JC-1) and TUNEL assay, the inflammatory factor secretion were assessed by ELISA assay, and the cellular and molecular mechanisms of DAla2GIP protection were investigated by using Real time-PCR, flow cytometry, Non- invasive calcium detection and western blotting techniques.

(1) DAPla2GIP prevents apoptosis of chondrocyte induced by H2O2. (2) DAla2GIP alleviated the inflammation of chondrocyte induced by H2O2. (3) DAla2GIP prevents chondrocyte apoptosis by inhibiting calcium influx of chondrocyte and regulating expression of Bcl-2 and Caspase-3induced by H2O2. (4) DAla2GIP inhibited the H2O2 mediated inflammation by up- regulating the expressions of Sox9 and Col2a1 and inhibiting PI3K/Akt/NF-κB pathway.

Our experimental results revealed that DAla2GIP prevents chondrocyte apoptosis by inhibiting calcium influx of chondrocyte and induced regulating expression of Bcl-2 and Casp ase-3by H2O2. Further, molecular biology experiments confirmed that DAla2GIP inhibited the H2O2 mediated inflammation vis up-regulating the expressions of Sox9 and Col2a1 and inhibiting PI3K/Akt/NF-κB pathway. The results demonstrate that DAla2GIP has protective properties in H2O2-induced chondrocyte injury, this finding shows that novel GIP analogues have the potential as a novel therapeutic for osteoarthritis patients.

中文摘要（谷歌機翻）

研究DAla2GIP對H2O2誘導(dǎo)的軟骨細胞凋亡和炎性因子分泌的保護作用，并探討DAla2GIP保護其的可能機制。

軟骨細胞分為以下四組：對照組，300μmH2O2、100μmM DAla2GIP和300μmH2O2n +100μpMDAla2GIP。用線粒體膜電位分析試劑盒（JC-1）和TUNEL法檢測軟骨細胞的凋亡，用ELISA法評估炎性因子的分泌，并通過實時PCR研究DAla2GIP保護的細胞和分子機制，流式細胞儀，無創(chuàng)鈣離子檢測和蛋白質(zhì)印跡技術(shù)。

（1）DAPla2GIP可防止H2O2誘導(dǎo)的軟骨細胞凋亡。（2）DAla2GIP減輕了H2O2誘導(dǎo)的軟骨細胞炎癥。 （3）DAla2GIP通過抑制軟骨細胞的鈣內(nèi)流并調(diào)節(jié)過氧化氫誘導(dǎo)的Bcl-2和Caspase-3的表達來防止軟骨細胞凋亡。（4）DAla2GIP通過上調(diào)Sox9和Col2a1的表達并抑制PI3K / Akt /NF-κB通路來抑制H2O2介導(dǎo)的炎癥。

我們的實驗結(jié)果表明，DAla2GIP通過抑制軟骨細胞的鈣內(nèi)流并誘導(dǎo)H2O2調(diào)節(jié)Bcl-2和Casp ase-3的表達來防止軟骨細胞凋亡。此外，分子生物學(xué)實驗證實，DAla2GIP通過上調(diào)Sox9和Col2a1的表達并抑制PI3K / Akt /NF-κB通路來抑制H2O2介導(dǎo)的炎癥。結(jié)果表明，DAla2GIP在H2O2誘導(dǎo)的軟骨細胞損傷中具有保護性，這一發(fā)現(xiàn)表明，新型GIP類似物具有作為骨關(guān)節(jié)炎患者的新型治療劑的潛力。

結(jié)果表明：100 pM DAla2-GIP組和Control組的Ca2+吸收速率并無顯著差異，平均值分別是1.94 pmol·cm-2·s-1和1.42 pmol·cm-2·s-1；經(jīng)300 μM H2O2處理后，Ca2+吸收速率明顯增加，平均值為139.61 pmol·cm-2·s-1；經(jīng)300 μM H2O2和100 pM DAla2-GIP共同處理后，Ca2+吸收速率明顯低于300 μM H2O2處理組，平均值為26.68 pmol·cm-2·s-1，說明DAla2-GIP抑制了H2O2誘導(dǎo)的Ca2+吸收。而Ca2+吸收是軟骨細胞凋亡早期的標(biāo)志。