xy9902对MC3T3-E1细胞的增殖和分化作用

目的研究化合物xy9902对成骨细胞MC3T3-E1的增殖和分化的影响,并初步探讨其机制。方法采用MTT比色法测定化合物对成骨细胞MC3T3-E1的增殖作用;通过硝基苯磷酸盐法测定细胞内碱性磷酸酶(A lkaline phosphatase,ALP)活性的变化,观察化合物对细胞分化的影响;用放射性配体结合法考察化合物与雌激素受体(Estrogen ic recep-tor,ER)的亲和力。结果化合物xy9902对成骨细胞有促增殖和促分化作用,这一作用可被tamoxifen阻断;xy9902与ER有亲和力,对ERα和ERβ的IC50分别为8.45×10-6mol.L-1和1.66×10-6mol.L-1。结论化合物xy9902对成骨细胞有促增殖和促分化作用,其作用机制可能与ER激动有关。     

黄芪多糖缓释纤维对成骨细胞MC3T3-E1增殖分化的影响

目的:研究黄芪多糖(AP)缓释纤维对成骨细胞MC3T3-E1增殖分化的影响。方法:将AP分别与左旋聚乳酸(PLLA)结合制备成AP质量浓度分别为0、25、50、100μg/ml的静电纺丝缓释纤维,即PLLA、PLLA/AP1、PLLA/AP2、PLLA/AP3,以异硫氰酸荧光素为指示剂于荧光显微镜下观察MC3T3-E1细胞在上述4种缓释纤维上的黏附情况;采用紫外分光光度法在490 nm波长处测定PLLA/AP1、PLLA/AP2、PLLA/AP3中AP的含量,考察其21 d内的体外释放情况;采用MTT法检测4种缓释纤维作用24、48、72 h时MC3T3-E1细胞的增殖情况;采用酶标仪法检测4种缓释纤维对MC3T3-E1细胞作用3、5、7 d时的碱性磷酸酶(ALP)活性表达情况。结果:镜下观察PLLA纤维连续,较多空隙,表面光滑;PLLA/AP1、PLLA/AP2、PLLA/AP3纤维呈纵横交错的三维、多空网络结构,且3种AP载药量下纤维形态未见明显改变。PLLA/AP1、PLLA/AP2、PLLA/AP3能持续释放AP 21 d,且最初的24 h内释药呈突释状态。与PLLA比较,PLLA/AP2、PLLA/AP3能促进MC3T3-E1细胞的增殖,PLLA/AP1仅作用48 h时能促进MC3T3-E1细胞的增殖,差异具有统计学意义(P<0.05);PLLA/AP1、PLLA/AP2、PLLA/AP3均能增强MC3T3-E1细胞中ALP活性表达,差异具有统计学意义(P<0.05),且与AP浓度呈正相关。结论:AP缓释纤维具有一定的缓释作用,且对MC3T3-E1细胞的增殖、分化具有剂量依赖性的促进作用。     

低氧激活自噬促进人间充质干细胞成骨分化的研究

目的 探讨低氧对人间充质干细胞(human mesenchymal stem cells,hMSCs)成骨分化的效应及分子机制。方法 在正常氧压(20% O₂)和低氧(5% O₂)条件下培养hMSCs;采用成骨分化诱导液(BDM)诱导hMSCs成骨分化;利用茜素红染色法考察细胞钙沉积情况;通过Western blotting检测细胞自噬相关蛋白的表达水平以及MAPK、PI3K-AKT-mTOR信号通路的激活情况。结果 低氧条件下,hMSCs钙沉积较常氧条件增强;BDM诱导hMSCs成骨分化过程伴随着LC3表达增加,抑制细胞自噬可以明显减弱低氧促进的细胞钙沉积;低氧促进的细胞发生钙沉积伴随着MAPK以及PI3K-AKT-mTOR信号通路的失活;抑制MAPK以及PI3K-AKT-mTOR信号通路有利于细胞自噬发生,进而促进hMSCs钙沉积。结论 低氧下可以通过激活细胞自噬来促进hMSCs成骨分化,抑制MAPK以及PI3K-AKT-mTOR信号通路可以进一步促进细胞自噬的发生,从而协同促进hMSCs成骨分化。     

葛根素对MC3T3-E1细胞增殖、分化和矿化及TRPM3 mRNA表达的影响

目的观察葛根素对小鼠成骨细胞MC3T3-E1细胞增殖、分化和矿化及TRPM3 mRNA表达的影响。方法分别采用CCK-8法、碱性磷酸酶(ALP)活性、茜素红染色测定葛根素对MC3T3-E1细胞增殖、成骨分化、矿化作用的影响。流式细胞术检测葛根素对MC3T3-E1细胞周期及细胞内钙离子浓度的影响。RT-PCR检测葛根素对TRPM3基因m RNA表达的影响。结果 0.1、1、10μmol·L~(-1)葛根素能明显促进MC3T3-E1细胞增殖,使G1期细胞比例减少,G_2+S期细胞比例增加,其中0.1μmol·L~(-1)浓度效果最为明显;与正常对照组相比较,0.1μmol·L~(-1)葛根素组细胞的ALP活性和矿化结节面积均明显提高;0.1μmol·L~(-1)葛根素组细胞的TRPM3 m RNA表达水平和细胞内钙离子浓度明显降低。结论葛根素可促进MC3T3-E1细胞的增殖、分化和矿化,可降低TRPM3 mRNA表达水平和细胞内钙离子浓度。     

异槲皮苷对MC3T3-E1成骨细胞增殖与分化的影响作用

目的研究异槲皮苷对体外培养MC3T3-E1成骨细胞增殖、分化的影响作用。方法以细胞矿化结节染色鉴定MC3T3-E1成骨细胞株骨矿化功能,以MTT法测定成骨细胞的增殖率,以试剂盒法测定细胞内碱性磷酸酶(ALP)的活性。结果在终浓度为1.08×10-6mol·L-1、1.08×10-7mol·L-1、1.08×10-8mol·L-1时,异槲皮苷能极显著促进MC3T3-E1成骨细胞增殖(P<0.01);终浓度为1.08×10-6mol·L-1时,异槲皮苷作用96h后能极显著提高细胞内ALP的活性(P<0.01)。结论一定浓度的异槲皮苷能够显著促进MC3T3-E1成骨细胞增殖和分化。     

二甲双胍通过自噬缓解氨诱导的星形胶质细胞老化

目的确定二甲双胍对氨致星形胶质细胞老化的保护作用,并从自噬角度探讨其抗老化机理。方法将星形胶质细胞分为对照组、氯化铵组、二甲双胍(250、500μmol·L~(-1))组。细胞先以二甲双胍预处理30 min,随后加入3 mmol·L~(-1)氯化铵共同作用72 h。以BeyoClick~(TM) EdU-488细胞增殖检测试剂盒检测DNA合成情况;以蛋白质免疫印迹法检测自噬和老化标志蛋白的表达。结果 3 mmol·L~(-1)氯化铵明显增加自噬蛋白LC3II、Beclin1和p62的表达。在Bafilomycin存在的情况下,氨可进一步诱导LC3Ⅱ表达的上调。二甲双胍预处理进一步增加氨诱导的LC3 II上调,但抑制氨诱导的p62增加。二甲双胍预处理缓解氨诱导的星形胶质细胞增殖抑制和p16蛋白的过表达。结论二甲双胍可通过促进细胞自噬缓解氨诱导的星形胶质细胞老化。     

卡托普利对MC3T3-E1细胞增殖、分化及Ⅰ型胶原mRNA表达的影响

目的观察卡托普利对MC3T3-E1细胞增殖、分化和Ⅰ型胶原基因表达水平影响。方法在MC3T3-E1细胞中加入不同浓度的卡托普利,应用MTT法、对硝基苯磷酸盐法、RT-PCR的方法观察卡托普利对MC3T3-E1细胞的增殖、碱性磷酸酶活性和Ⅰ型胶原mRNA表达的影响。结果 10-11 mol.L-1浓度的卡托普利作用24 h能明显促进MC3T3-E1细胞增殖,作用3 d能明显促进MC3T3-E1细胞表达碱性磷酸酶。卡托普利可刺激MC3T3-E1细胞表达Ⅰ型胶原,以10-11 mol.L-1作用最强。结论卡托普利有促进MC3T3-E1细胞增殖、促进碱性磷酸酶表达和增加Ⅰ型胶原mRNA表达的作用。     

二甲双胍通过改善自噬功能障碍保护多柔比星诱导的心肌细胞损伤

目的 探讨二甲双胍(metformin,Met)保护DOX诱导的心肌损伤的作用机制。方法 ①H9C2细胞经0.1~10 mmol·L^-1Met预处理后加入1 μmol·L^-1 DOX处理24 h,MTT法检测细胞存活率,Annexin V-PI染色后流式细胞技术检测细胞凋亡率,使用ROS试剂盒检测细胞内ROS蓄积情况;②使用Western blotting检测0.1,0.3,3 mmol·L^-1 Met对DOX激活自噬水平的调节作用,并使用25 μmol·L^-1 AG-126考察ERK信号通路调节DOX诱导心肌细胞损伤中的作用;③10 nmol·L^-1 BafA1用于探索Met恢复DOX阻断心肌细胞自噬流的研究,流式细胞技术检测吖啶橙细胞内溶酶体pH的变化。结果 DOX(1 μmol·L^-1)的接触会使H9C2细胞的存活率显著下降(P<0.05),同时心肌细胞内ROS累积增加(P<0.05),凋亡细胞比例升高(P<0.05),不同浓度的Met可以有效缓解DOX升高的H9C2细胞内ROS和凋亡细胞比率(P<0.05),从而增加心肌细胞存活率(P<0.05)。DOX(1 μmol·L^-1)处理H9C2细胞6 h能够有效激活细胞自噬,损伤心肌细胞。通过AG-126干预可知,DOX诱导的心肌细胞自噬与ERK分子的激活相关,3 mmol·L^-1 Met可以下调ERK的磷酸化水平(P<0.05),从而降低DOX诱导的心肌细胞自噬。吖啶橙染色和Western blotting结果显示,与自噬流阻断剂BafA1处理的H9C2细胞比较,DOX同样增加H9C2细胞内溶酶体pH(P<0.05),使心肌细胞自噬功能异常,增加细胞凋亡程度。结论 DOX损伤心肌细胞是通过上调自噬水平并诱发自噬功能障碍引起心肌细胞凋亡,Met下调ERK磷酸化水平,缓解DOX破坏的心肌细胞自噬障碍,保护心肌细胞免受DOX诱导的伤害。     

二甲双胍调节自噬保护亚急性衰老大鼠睾丸功能的作用

目的:研究二甲双胍(Met)对D-半乳糖构建的亚急性衰老模型大鼠睾丸功能的影响及其分子调控机制。方法:颈部皮下注射D-半乳糖制备亚急性衰老大鼠模型。次月予以Met溶液灌胃治疗,每周监测大鼠的体重,测定大鼠睾丸重量、睾丸指数;ELISA法检测大鼠血清睾酮(testosterone, T)、卵泡刺激素(FSH)、黄体生成素(LH)和雌二醇(E₂)水平;HE染色法观察睾丸形态;免疫组化染色检测衰老相关蛋白[β-半乳糖苷酶(β-gal)、p16和p21]、睾丸自噬相关蛋白[磷酸酶张力蛋白同源物诱导激酶1(PINK1)、Parkin、自噬效应蛋白(Beclin-1)、微管相关蛋白1轻链3(LC3)和p62]和睾酮合成关键酶[类固醇激素合成急性调节蛋白(StAR)、细胞色素侧链裂解酶(CYP11A1)和17-β-羟基类固醇脱氢酶3(HSD17β3)]的表达情况,并用Western blot检测上述蛋白的表达量。结果:与对照组相比,衰老模型组和Met组大鼠体重整体呈下降趋势;衰老模型组睾丸重量及指数下降(P<0.01),Met干预后显著上升(P<0.001)。衰老模...     

罗格列酮对体外培养小鼠前成骨细胞系MC3T3-E1生长与分化的影响研究

目的:研究罗格列酮对体外培养小鼠前成骨细胞系MC3T3-E1生长与分化的影响。方法:以小鼠MC3T3-E1作为药物筛选的细胞模型,分别加入1、2、5、10μmo·lL-1罗格列酮干预,MTT法测定细胞活性并计算生长抑制率;流式细胞术检测细胞凋亡率;免疫组化法分析细胞中促凋亡因子Bax和抗凋亡因子Bcl-2蛋白的表达;测定细胞中分化指标碱性磷酸酶(ALP)的活性。设立只加入培养基处理的空白对照组。结果:与空白对照组比较,罗格列酮各浓度组生长抑制率、细胞凋亡率升高(P均<0.05),Bax表达增强、Bcl-2表达减弱、ALP活性下降(P均<0.05),且呈浓度依赖性。结论:罗格列酮可抑制MC3T3-E1细胞生长及分化,并诱导其凋亡;而Bax/Bcl-2可能参与凋亡的发生,并可能起关键调控作用。     

Fluoride-induced c-Fos expression in MC3T3-E1 osteoblastic cells

Excessive systemic exposure to fluoride leads to disturbances of bone homeostasis. c-Fos is known to be essential in bone development by affecting osteoblast and osteoclast differentiation. In this study, we examined the effects of fluoride exposure on c-Fos expression and its regulatory signaling pathways in MC3T3-E1 mouse osteoblast cell line. c-fos mRNA level, c-Fos protein level and c-Fos DNA-binding activity were markedly increased, with a peak at 2 or 4?h, in MC3T3-E1 cells exposed to sodium fluoride (NaF). Fra-1 protein, another member of Fos family, was also elevated, whereas FosB and Fra-2 proteins remained unchanged. NaF further induced phosphorylation of mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated protein kinase 1/2 (ERK1/2), ERK5, c-Jun NH₂-terminal kinase and p38. NaF-induced expression of c-Fos protein was markedly suppressed with U0126, the inhibitor of both activated and non-activated forms of MAPK/ERK kinase 1/2 (MEK1/2) and BIX02189, the MEK5 inhibitor, but partially with SP600125, the JNK inhibitor and SB203580, the p38 inhibitor. Therefore, ERK1/2 and ERK5 signal transduction pathways are important for accumulating c-Fos. siRNA targeting against the mouse c-fos gene further enhanced NaF-induced up-regulation of osteoprotegerin (OPG), an inhibitor of osteoclastogenesis, suggesting that c-Fos might negatively regulate OPG expression induced by fluoride in osteoblastic cells.     

Costunolide stimulates the function of osteoblastic MC3T3-E1 cells

The effect of costunolide on the function of osteoblastic MC3T3-E1 cells was studied. Costunolide significantly increased the growth of MC3T3-E1 cells and caused a significant elevation of alkaline phosphatase (ALP) activity, collagen content, and mineralization in the cells (P<0.05). The effect of costunolide in increasing cell growth was completely prevented by the presence of ICI182780, LY294002, PD98059, rotlerin, or glibenclamide, suggesting that the effect of costunolide might be partly mediated from estrogen receptor (ER), PI3K, ERK, protein kinase C (PKC) and mitochondrial ATP-sensitive K(+) channel. The effect of costunolide in increasing ALP activity was prevented by the presence of ICI182780, PD98059, SB203580, or rotrelin, suggesting that the effect of costunolide on ALP activity might be mediated from ER, ERK, p38, and PKC. The effect of costunolide in increasing collagen content was prevented by the presence of LY294002, PD98059, SB203580, SP600125, or rotrelin, suggesting that the effect of costunolide on collagen synthesis might be mediated from PI3K, ERK, p38, JNK, and PKC. Moreover, cotreatment of ICI182780 or LY294002 inhibited costunolide-mediated upregulation of mineralization, suggesting that the induction of mineralization by costunolide is associated with increased activation of ER and PI3K. Our data indicate that the enhancement of osteoblast function by costunolide may result in the prevention for osteoporosis.     

Mitochondrial defects and cytotoxicity by antimycin A on cultured osteoblastic MC3T3-E1 cells

Antimycin A (AMA), which inhibits complex III of the electron transport system, has been used as a reactive oxygen species (ROS) generator in biological systems. We investigated the effects of AMA on various parameters related to mitochondrial function in osteoblastic MC3T3-E1 cells. Here, we show that AMA-induced cell death was accompanied by the loss of ATP, complex I and IV activities, and mitochondrial membrane potential. Moreover, AMA stimulated oxidative stress and induced cytochrome c release from mitochondria in osteoblasts. Our data support AMA-induced death in osteoblasts via a mitochondria-dependent pathway. These biochemical changes in mitochondria were effectively prevented upon pre-treatment with ROS scavengers, indicating that ROS plays a critical role as an upstream controller in the AMA-induced cell dysfunction.     

The licorice root derived isoflavan glabridin increases the function of osteoblastic MC3T3-E1 cells

Glabridin, an isoflavan purified from licorice root, exhibits diverse biological activities, including estrogen-like activity. To investigate the bioactivities of glabridin, which act on bone metabolism, the effects of glabridin on the function of mouse osteoblastic cell line (MC3T3-E1) and the production of local factors in osteoblasts were studied. Glabridin (1-10microM) significantly increased the growth of MC3T3-E1 cells and caused a significant elevation of alkaline phosphatase (ALP) activity, collagen content and osteocalcin secretion in the cells (P<0.05). The effect of glabridin (10microM) in increasing ALP activity and collagen content was completely prevented by the presence of 10(-6)M cycloheximide and 10(-6)M tamoxifen, suggesting that glabridin's effect results from a newly synthesized protein component and might be partly involved in estrogen action. Then, the effects of glabridin on the TNF-alpha-induced apoptosis and production of prostaglandin E2 (PGE2) and nitric oxide (NO) in osteoblasts were examined. Treatment with glabridin (1-10microM) prevented apoptosis induced by TNF-alpha (10(-10)M) in osteoblastic cells. Moreover, glabridin (50microM) decreased the 10(-10)M TNF-alpha-induced production of PGE2 and NO in osteoblasts. Our data indicate that the enhancement of osteoblast function by glabridin may result in the prevention for osteoporosis and inflammatory bone diseases.     

Protective effect of diazoxide against antimycin A-induced mitochondrial dysfunction in osteoblastic MC3T3-E1 cells

Treatment of various types of cells with diazoxide has been shown to precondition cells to subsequent injuries and inhibit cell death. In this study, the protective effects of diazoxide against pharmacological inhibition of the respiratory chain were studied using osteoblastic MC3T3-E1 cells treated with antimycin A (AMA), which inhibits complex III of the electron transport system. Diazoxide restored mitochondrial membrane potential dissipation, inactivation of complex IV, ATP loss, and intracellular calcium elevation that was induced by AMA treatment, and prevented cell death. The results imply that diazoxide protects osteoblasts from AMA-induced cell death via improved mitochondrial function. Moreover, diazoxide scavenged mitochondrial superoxide anions generated by AMA, and prevented nitrotyrosine increase and thioredoxin reductase inactivation induced by AMA, suggesting that diazoxide may be useful to protect mitochondria from a burst of oxidative stress. Our results demonstrate that diazoxide may reduce or prevent osteoblasts degeneration in osteoporosis.     

Bezafibrate enhances proliferation and differentiation of osteoblastic MC3T3-E1 cells via AMPK and eNOS activation

Aim:

To investigate the effects of bezafibrate on the proliferation and differentiation of osteoblastic MC3T3-E1 cells, and to determine the signaling pathway underlying the effects.

Methods:

MC3T3-E1 cells, a mouse osteoblastic cell line, were used. Cell viability and proliferation were examined using MTT assay and colorimetric BrdU incorporation assay, respectively. NO production was evaluated using the Griess reagent. The mRNA expression of ALP, collagen I, osteocalcin, BMP-2, and Runx-2 was measured using real-time PCR. Western blot analysis was used to detect the expression of AMPK and eNOS proteins.

Results:

Bezafibrate increased the viability and proliferation of MC3T3-E1 cells in a dose- and time-dependent manner. Bezafibrate (100 μmol/L) significantly enhanced osteoblastic mineralization and expression of the differentiation markers ALP, collagen I and osteocalcin. Bezafibrate (100 μmol/L) increased phosphorylation of AMPK and eNOS, which led to an increase of NO production by 4.08-fold, and upregulating BMP-2 and Runx-2 mRNA expression. These effects could be blocked by AMPK inhibitor compound C (5 μmol/L), or the PPARβ inhibitor GSK0660 (0.5 μmol/L), but not by the PPARα inhibitor MK886 (10 μmol/L). Furthermore, GSK0660, compound C, or N^G-nitro-L-arginine methyl ester hydrochloride (L-NAME, 1 mmol/L) could reverse the stimulatory effects of bezafibrate (100 μmol/L) on osteoblast proliferation and differentiation, whereas MK886 only inhibited bezafibrate-induced osteoblast proliferation.

Conclusion:

Bezafibrate stimulates proliferation and differentiation of MC3T3-E1 cells, mainly via a PPARβ-dependent mechanism. The drug might be beneficial for osteoporosis by promoting bone formation.     

染料木素促成骨样细胞增殖作用及其机制研究

目的观察染料木素(genistein)对成骨样细胞MC3T3-E1细胞增殖及骨形成蛋白-2(BMP-2)、β-连环素(β-catenin)表达的影响。方法培养成骨样细胞MC3T3-E1,加入不同浓度的染料木素(1×10-10、1×10-9、1×10-8、1×10-7、1×10-6和1×10-5mol·L-1),以1×10-9mol·L-1雌激素(β-estradiol,E2)作为阳性对照组,采用MTT比色试验法和碱性磷酸酶(ALP)活性检测法,观察染料木素作用后MC3T3-E1的增殖及分化情况,以Westernblot方法检测成骨样细胞中BMP-2和β-catenin蛋白的表达。结果染料木素可促进MC3T3-E1细胞增殖,染料木素作用后细胞的ALP值也明显升高,呈浓度依赖性;染料木素可增加BMP-2和β-catenin表达,且呈浓度依赖性。结论染料木素促进MC3T3-E1细胞增殖与分化,可通过调节BMP-2和Wnt/β-catenin信号通路而影响成骨样细胞的活性。     

淫羊藿苷抑制亮氨酸拉链蛋白表达调节糖皮质激素诱导的MC3T3-E1成骨基因的表达失衡

目的考察成骨细胞MC3T3-E中亮氨酸拉链蛋白（GILZ）的表达与淫羊藿苷（icraiin,ICR）和糖皮质激素地塞米松（dexamethasone,DEX）之间的关系以及对部分成骨相关基因的表达影响。方法将诱导成熟分化的MC3T3-E1细胞分为3组,分别为DEX组、ICR组以及ICR＋DEx组,通过Real—TimeRT—PCR来检测不同组中GILZ、骨保护素（OPG）、破骨细胞分化因子（RANKL）、骨钙素（Oc）和碱性磷酸酶（ALP）mRNA表达。结果DEX能够提升GILZ、RANKL和ALP的表达,降低OPG、OC的表达,提高RANKL／OPG表达比率。ICR能够抑制G[LZ、RANKL和ALP的表达,提升OPG、OC的表达,降低RANKL／OPG表达比率。并且ICR能够抑制DEX诱导的GILZ、RANKL和ALP表达升高,逆转DEX诱导的OPG、OC的表达抑制。同时显著降低了RANKL／OPG表达比率。结论ICR通过抑制GILZ的mRNA表达,降低RANKL／OPG的表达比率,抑制破骨细胞成熟激活。ICR通过抑制ALP表达和提高OC表达提高成骨细胞的增殖能力。     

胶原蛋白肽经由HO-1途径保护H2O2诱导的MC3T3-E1细胞损伤△*

目的 骨质疏松症与氧化应激和活性氧（ROS）的产生密切相关,胶原蛋白肽具有潜在的抗氧化作用,其作用机理尚不清楚,因此,本研究在胶原蛋白肽对过氧化氢（H2O2）诱导的MC3T3-E1小鼠前成骨细胞氧化应激的保护作用的基础上,探讨其分子作用机制。方法 实验分为正常组,H2O2组,胶原蛋白肽低、中、高剂量组(10, 100, 500 g?L-1)。胶原蛋白肽各组加入相应浓度的药物预处理24 h后,与H2O2组一起加入400 μmol?L-1 H2O2孵育24 h,空白对照组正常培养。CCK 8和乳酸脱氢酶（LDH）的释放检测细胞毒性。抗氧化试剂盒检测细胞内活性氧（ROS）、谷胱甘肽过氧化物酶（GSH）和丙二醛(MDA)含量的变化,Western blot和RT-PCR分别检测细胞内HO-1蛋白及mRNA的表达水平。结果 胶原蛋白肽能够上调H2O2诱导的细胞存活率,以剂量依赖的方式显著降低H2O2诱导的氧化损伤。胶原蛋白肽能够及时清除细胞内的活性氧,显著上调HO-1的基因表达,提高GSH、MDA的活性,减轻脂质过氧化反应。结论 胶原蛋白肽通过激活HO-1基因表达水平,提高抗氧化活性,对H2O2诱导MC3T3-E1细胞的氧化损伤发挥保护作用。