共查询到19条相似文献，搜索用时 812 毫秒
1.
目的:探讨表没食子儿茶素没食子酸脂(EGCG)对高糖培养的系膜细胞(GMCs)增殖及周期素激酶抑制剂p27蛋白表达的作用。方法:以大鼠肾系膜细胞为实验对象,将GMCs分成6组,分别刺激48h后,用四甲基偶氮唑蓝(MTT)测定GMCs增殖情况,Westernblot法测定p27蛋白表达。结果:作用48h后,高糖明显诱导GMCs增殖并上调p27蛋白表达,不同浓度的EGCG能抑制高糖诱导的细胞增生,并抑制p27蛋白表达。结论:EGCG能抑制高糖诱导的GMCs增殖,并下调p27蛋白表达,提示EGCG可通过抑制p27表达而减少细胞外基质的积聚,延缓糖尿病肾小球肥大和肾小球硬化。 相似文献
2.
探究茶黄素(TF1)对人肝癌Bel-7402细胞的影响,并阐明其作用机制。通过CCK-8检测细胞活力,用平板克隆形成试验检测细胞增殖能力,细胞划痕愈合试验和Transwell小室法检测细胞迁移,用流式细胞术检测细胞凋亡,Western blot检测细胞凋亡相关蛋白(Bax、Bcl-2、PARP)、迁移相关蛋白(E-cad、N-cad、Vimentin、MMP9)和信号通路相关蛋白(TGF-β、smad3、p-smad3)表达水平。结果表明,不同剂量TF1均可抑制Bel-7402细胞的增殖和迁移,促进其凋亡,并且存在剂量依赖性,剂量越大,抑制作用越强(P<0.05)。与对照组相比,试验组Bax、E-cad蛋白表达水平较高,Bcl-2、PARP,N-cad、Vimentin、MMP9、TGF-β、smad3、p-smad3表达水平较低(P<0.05)。茶黄素可能通过TGF-β信号通路抑制肝癌Bel-7402细胞的增殖、迁移,且促进其凋亡。 相似文献
3.
为了探讨大豆异黄酮对肝癌移植瘤血管生成的抑制作用,建立小鼠H22肝癌皮下移植瘤模型。用大豆异黄酮干预10 d,利用免疫组化染色法检测肿瘤组织内微血管密度,利用免疫印迹法检测肿瘤组织内血管内皮细胞生长因子(VEGF)、血管内皮细胞生长因子受体2(VEGFR2)和缺氧诱导因子-1α(HIF-1α)的表达,酶联免疫吸附测定(ELISA)法检测转化生长因子-β1(TGF-β1)和基质金属蛋白酶2(MMP2)的水平。结果显示,大豆异黄酮组移植瘤细胞生长受到抑制,细胞坏死较严重。与模型组比较,大豆异黄酮组肿瘤组织内微血管密度降低;VEGF、VEGFR2和HIF1α的蛋白表达降低;TGF-β1及MMP2蛋白表达下降。提示,大豆异黄酮对小鼠H_(22)移植瘤组织的血管生成具有抑制作用,机制可能与下调移植瘤组织VEGF和TGF-β1蛋白表达有关。 相似文献
4.
豆豉对早期动脉粥样硬化大鼠主动脉平滑肌细胞凋亡的影响 总被引：7，自引：2，他引：5
观察豆豉对早期动脉粥样硬化大鼠主动脉平滑肌细胞凋亡及相关凋亡基因突变型p53和Fas蛋白表达的调节作用,以探讨其机制.采用高脂饲料喂养法建立大鼠早期动脉粥样硬化模型,同时连续10周灌胃给予豆豉提取物进行干预.末次给药后处死动物,光镜下观察血管平滑肌细胞的形态,透射电镜观察超微结构,采用流式细胞术检测细胞凋亡率以及凋亡相关基因突变型p53和Fas蛋白的表达.模型对照组主动脉平滑肌细胞的凋亡率及增值指数(FI)明显高于正常对照组(P＜0.05),053蛋白表达上调;豆豉干预组(20 g生药·kg-1,dO g生药·kg-1)大鼠主动脉平滑肌细胞的凋亡率明显高于模型对照组(P＜0.05),增殖指数明显低于模型对照组(P＜0.05),Fas蛋白表达上调(P＜0.05),p53蛋白表达下调(P＜0.05),光镜及透射电镜可见主动脉损伤明显较模型对照组改善.豆豉可调节早期动脉粥样硬化大鼠血管平滑肌细胞凋亡与增殖的平衡,其机制可能与调节突变型p53和Fas蛋白的表达有关. 相似文献
5.
体外分离培养SD雄性大鼠膝关节软骨细胞,经甲苯胺蓝及Ⅱ型胶原(Col Ⅱ)免疫荧光染色鉴定后,加入白介素-1β(IL-1β)诱导建立骨关节炎(OA)细胞模型,探讨茶黄素双没食子酸酯(TFDG)对OA软骨细胞的保护作用。细胞形态观察发现TFDG能明显改善OA软骨细胞形态。实时荧光定量PCR(Real-time PCR)结果显示,TFDG不仅可以上调软骨细胞分子标志物Col Ⅱ mRNA的表达,还可以下调炎症因子IL-1β、IL-6mRNA的表达。酶联免疫吸附实验(ELISA)检测结果进一步表明TFDG可明显降低炎症因子的分泌。免疫印迹(Western blot)检测结果证明,TFDG预干扰可降低炎症诱导酶环氧化酶COX-2蛋白表达量。这些结果说明TFDG通过减弱炎症反应,从而对IL-1β体外诱导大鼠软骨细胞炎性损伤起到保护作用。 相似文献
6.
目的探讨鹿茸多肽(velvet antler peptide,VAP)预处理对叔丁基过氧化氢(TBHP)诱导H9c2大鼠心肌细胞损伤及凋亡的影响。方法采用含10%胎牛血清(FBS)培养液(DMEM)传代培养细胞7d后,将H9c2心肌细胞分为空白对照组(Blank control group)、空白血清组(Blank serum group)、TBHP组(TBHP group)、100 mg·kg^(-1)VAP低剂量含药血清组(TBHP+VAPLgroup)、400 mg·kg^(-1) VAP高剂量含药血清组(TBHP+VAPHgroup)。正常对照组不做任何处理,其余给药组给予VAP处理24h后,给予200μmol·L^(-1)TBHP处理。MTT法检测各组细胞存活率;Hochst染色法检测各组细胞凋亡情况;Western blotting法检测心肌细胞Bax、Bcl-2、Caspase-3蛋白表达水平。结果MTT检测结果表明,与TBHP组比较,VAP高和低剂量组的H9c2细胞活性升高(P<0.01)。Hoechst染色法结果显示,与空白对照组比较,TBHP组的活细胞减少;与TBHP组比较,VAP高和低剂量组的活细胞增多。Western blotting法检测结果表明,与空白对照组比较,TBHP组上调心肌细胞Bax、Caspase-3蛋白表达水平,降低Bcl-2蛋白表达水平(P<0.05);与TBHP组比较,VAP高和低剂量组降低Bax、Caspase-3蛋白表达水平,升高Bcl-2蛋白表达水平(P<0.05)。结论VAP含药血清预处理可保护TPHP诱导的H9c2细胞心肌损伤。通过降低心肌细胞中Caspase-3蛋白的表达或抑制其活性,增加Bcl-2蛋白的表达,降低Bax蛋白的表达,上调Bcl-2/Bax,从而抑制心肌细胞凋亡。 相似文献
7.
EGCG是一种抗氧化、抗炎症的天然活性成分，目前关于EGCG的抗氧化和抗炎症作用在糖尿病肾损伤中的作用及调节机制研究较少。采用不同剂量的EGCG干预非肥胖型糖尿病Goto-Kakizaki(GK)大鼠以探究EGCG对糖尿病大鼠肾损伤的作用和机制。试验周期为4周，监测试验期内大鼠的平均体质量和日平均摄食量，并在试验结束后取血清和肾脏组织，检测大鼠肾功能、肾脏病理指标、氧化应激和炎症指标以及Nrf2-Keap1/MAPK信号通路相关基因表达水平。试验表明，EGCG能够有效改善GK大鼠肾脏形态损伤，显著降低血肌酐、尿素氮和肾脏丙二醛含量，提高肾脏超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶等抗氧化酶活性，抑制促炎因子单核细胞趋化蛋白-1和白介素-1β的释放水平，调节与抗氧化应激相关的Nrf2-Keap1/MAPK信号通路的Nrf2、Keap1、JNK、NF-κB、P38基因表达水平，且在试验范围内，高剂量的改善效果优于低剂量。以上结果表明，EGCG对大鼠糖尿病导致的肾损伤有一定的改善作用，其作用机理可能与Nrf2-Keap1/MAPK信号通路介导的抗氧化应激有关。 相似文献
8.
4-羟基-3-甲基-2-(E)-丁烯基-4-磷酸还原酶(4-hydroxy-3-methyl-2-(E)-butenyl-4-diphosphate reductase,HDR)是异戊烯基焦磷酸合成途径之一甲基赤藓糖磷酸(methylerythritol phosphate,MEP)途径中的最后一个酶,催化4-羟基-3-甲基-(2E)-丁烯基-4-磷酸生成异戊烯基焦磷酸.根据笔者从橡胶树中克隆的HDR基因(命名为HbHDR,GenBank登录号:EU881977)序列,构建了HbHDR的原核表达载体,并在大肠杆菌中诱导表达获得融合表达蛋白.将融合蛋白免疫新西兰大白兔,制备HbHDR的高效价特异的多克隆抗体.Western-blot分析表明,HbHDR存在于乳管细胞的橡胶粒子和C-乳清中. 相似文献
9.
干旱胁迫对燕麦叶片气孔和叶肉细胞超微结构的影响 总被引：1，自引：0，他引：1
为了解干旱后燕麦解剖结构的变化,以燕麦品种白燕2号为材料,通过盆栽控水试验,设置正常供水、轻度干旱和重度干旱三个不同水分处理(土壤含水量分别为田间持水量的75%、60%和45%),研究了干旱胁迫对燕麦叶片渗透调节物质含量、气孔和叶肉细胞超微结构的影响。结果表明,正常水分条件(对照)下,燕麦叶片脯氨酸和可溶性糖含量较低,表皮细胞皱褶,气孔关闭或微张,叶肉细胞内细胞器形状规则,结构清晰。与对照相比,轻度干旱胁迫下,燕麦叶片脯氨酸和可溶性糖含量增加,叶片表皮细胞饱满,气孔开启度较大,叶绿体形状变圆,近球状,线粒体外被膜膨胀,但结构未见明显损伤;重度干旱胁迫下,叶片脯氨酸和可溶性糖含量极显著增加,表皮细胞干瘪,气孔保卫细胞膨胀,气孔关闭,气孔器下陷。重度干旱胁迫下,燕麦叶绿体和线粒体受到的损伤较大,叶绿体内基粒、基质类囊体降解,出现较大的空腔;线粒体外被膜断裂,内含物流失;细胞核染色质凝聚,叶绿体之间出现嵌合现象。因此,干旱胁迫能诱导燕麦叶片渗透调节物质的积累和细胞超微结构的改变,渗透调节物质增幅和细胞超微结构的破坏程度随着土壤有效水分含量的降低而上升,但在细胞超微结构上也出现抗性反应,表明燕麦具有较强的抗旱性。 相似文献
10.
《大豆科学》2020,(4)
为研究大豆异黄酮对过氧化氢所致L02细胞凋亡的抑制作用及其可能机制,以过氧化氢诱导L02细胞制备L02肝细胞凋亡模型。用Hoechst 33342荧光染色技术观察L02细胞核形态变化,用原位末端标记(TUNEL)技术观察L02细胞凋亡情况,采用免疫印迹法检测L02细胞中Caspase-3活性片段(Cleaved caspase-3)、B细胞淋巴瘤/白血病-2(Bcl-2)、Bcl-2相关X蛋白(Bax)、聚腺苷二磷酸核糖聚合酶活性片段(Cleaved PARP)表达,以及c-Jun氨基末端激酶(JNK)和核转录因子-κB(NF-κB)活化情况。结果显示:过氧化氢处理L02细胞能使细胞核Hoechst染色和TUNEL染色增强,提示L02细胞凋亡增多。同时,过氧化氢上调L02细胞Cleaved caspase-3、Cleaved PARP表达(P0.05)、Bax/Bcl-2比值(P0.05)和NF-κB p65核转位水平(P0.05)。与损伤组比较,大豆异黄酮组L02细胞凋亡显著减少,Cleaved caspase-3和Cleaved PARP表达量、Bax/Bcl-2比值和NF-κB p65核转位水平均降低(P0.05)。结果表明大豆异黄酮能抑制过氧化氢所致L02细胞凋亡,其作用可能与NF-κB通路有关。 相似文献
11.
感染赤霉病菌后小麦穗组织蛋白的氧化交联 总被引：1，自引：0，他引：1
为探究细胞壁组成蛋白在抗赤霉病中的作用，对接种赤霉病茵后小麦抗、感品种穗组织中离子结合型蛋白进行了分析。样品过氧化物酶比活力测定结果显示，高抗品种苏麦3号和望水白在接种赤霉病茵孢子后的6d内，过氧化物酶(POD)比活力明显高于对照，中抗品种扬麦158比对照也略有增加，而感病品种宁麦6号和安农8455则与对照无差异。用凝胶层析的方法分析了抗赤霉病程度不同的5个小麦品种穗组织盐溶成份。结果表明，2个高抗品种在接种病原物或过氧化氢处理后．洗脱体积为8ml的蛋白质(P8)的吸收峰明显增高．而在感病品种中P8蛋白变化不明显。高抗品种的对照样品在过氧化氢水浴(35℃)处理后，P8峰有所提高，表现出与赤霉病茵接种处理一致的趋势。 相似文献
12.
Inhibitory effects of Ecklonia cava extract on high glucose-induced hepatic stellate cell activation
Nonalcoholic steatohepatitis (NASH) is a disease closely associated with obesity and diabetes. A prevalence of type 2 diabetes and a high body mass index in cryptogenic cirrhosis may imply that obesity leads to cirrhosis. Here, we examined the effects of an extract of Ecklonia cava, a brown algae, on the activation of high glucose-induced hepatic stellate cells (HSCs), key players in hepatic fibrosis. Isolated HSCs were incubated with or without a high glucose concentration. Ecklonia cava extract (ECE) was added to the culture simultaneously with the high glucose. Treatment with high glucose stimulated expression of type I collagen and α-smooth muscle actin, which are markers of activation in HSCs, in a dose-dependent manner. The activation of high glucose-treated HSCs was suppressed by the ECE. An increase in the formation of intracellular reactive oxygen species (ROS) and a decrease in intracellular glutathione levels were observed soon after treatment with high glucose, and these changes were suppressed by the simultaneous addition of ECE. High glucose levels stimulated the secretion of bioactive transforming growth factor-β (TGF-β) from the cells, and the stimulation was also suppressed by treating the HSCs with ECE. These results suggest that the suppression of high glucose-induced HSC activation by ECE is mediated through the inhibition of ROS and/or GSH and the downregulation of TGF-β secretion. ECE is useful for preventing the development of diabetic liver fibrosis. 相似文献
13.
In the present study, we fabricated two-component extracellular matrix protein patterned substrates with fibronectin (FN) and laminin (LN) because of our interest in the mechanism of axonal regeneration and injury in the central and peripheral nervous systems. The authors investigated how the patterning order and method of attachment affected the spatial distribution and biological activity of the immobilized proteins. Micro-contact printing (μCP) techniques in concert with reactive surface chemistry were used to modify glass substrates with one- and two-component films of FN and LN, including micrometer-scale patterns of FN and LN. The composition and spatial distributions of both proteins on the patterned surfaces were characterized by x ray photoelectron spectroscopy, epi-fluorescence microscopy, atomic force microscopy, and time-of-flight secondary-ion mass spectrometry. The authors also characterized the biological activity of the top-most protein layer in a two-layer protein system as well as the ability of the top-most protein layer to mask the biological activity of an underlying protein layer using a fluorescence-based enzyme-linked immunosorbent assay. The order of protein deposition significantly affected the relative biological activity of the upper-most and underlying immobilized proteins. As a result of these optimization studies, maximum biological activity per surface protein was achieved by first immobilizing FN from solution, followed by μCP of LN on the FN. Addition of μCP LN films was able to mask ～84% of the underlying FN activity, whereas μCP FN films were only able to mask ～27% of the underlying LN activity. 相似文献
14.
Hyun Soo Park Hye Jin Hwang Gi-Young Kim Hee-Jae Cha Wun-Jae Kim Nam Deuk Kim Young Hyun Yoo Yung Hyun Choi 《Marine drugs》2013,11(7):2347-2364
The present study investigated possible mechanisms on the apoptosis induction of human leukemic cells by fucoidan, a sulfated polysaccharide found in marine algae. Fucoidan treatment of cells resulted in inhibition of growth and induction of apoptosis, as measured by 3-(4,5-dimetylthiazol-2-yl)-2,5-diphenyl-tetrazolium (MTT) assay, fluorescence microscopy, DNA fragmentation, and flow cytometry analysis. The increase in apoptosis was associated with the proteolytic activation of caspases, Bid cleavage, insertion of pro-apoptotic Bax into the mitochondria, release of cytochrome c from mitochondria to cytosol, and loss of mitochondria membrane potential (MMP) in U937 cells. However, apoptosis induced by fucoidan was attenuated by caspase inhibitors, indicating that fucoidan-induced apoptosis was dependent on the activation of caspases. Furthermore, fucoidan treatment effectively activated the p38 mitogen-activated protein kinase (MAPK) and p38 MAPK inhibitor, SB203580, and significantly reduced fucoidan-induced apoptosis through inhibition of Bax translocation and caspases activation, suggesting that the activation of p38 MAPK may play a key role in fucoidan-induced apoptosis. In addition, the authors found fucoidan-induced significantly attenuated in Bcl-2 overexpressing U937 cells, and pretreatment with fucoidan and HA 14-1, a small-molecule Bcl-2 inhibitor, markedly increased fucoidan-mediated apoptosis in Bcl-2 overexpressing U937 cells. Our findings imply that we may attribute some of the biological functions of p38 MAPK and Bcl-2 to their ability to inhibit fucoidan-induced apoptosis. 相似文献
15.
Excessive alcohol consumption can lead to brain tissue damage and cognitive dysfunction. Acetaldehyde, the most toxic metabolite of ethanol, mediates the brain tissue damage and cognitive dysfunction induced by chronic excessive alcohol consumption. In this study, the effect of astaxanthin, a marine bioactive compound, on acetaldehyde-induced cytotoxicity was investigated in SH-SY5Y cells. It was found that astaxanthin protected cells from apoptosis by ameliorating the effect of acetaldehyde on the expression of Bcl-2 family proteins, preventing the reduction of anti-apoptotic protein Bcl-2 and the increase of pro-apoptotic protein Bak induced by acetaldehyde. Further analyses showed that astaxanthin treatment inhibited acetaldehyde-induced reduction of the levels of activated Akt and cyclic AMP-responsive element binding protein (CREB). Astaxanthin treatment also prevented acetaldehyde-induced increase of the level of activated p38 mitogen-activated protein kinase (MAPK) and decrease of the level of activated extracellular signal-regulated kinases (ERKs). Activation of Akt/CREB pathway promotes cell survival and is involved in the upregulation of Bcl-2 gene. P38MAPK plays a critical role in apoptotic events while ERKs mediates the inhibition of apoptosis. Thus, astaxanthin may inhibit acetaldehyde-induced apoptosis through promoting the activation of Akt/CREB and ERKs and blocking the activation of p38MAPK. In addition, astaxanthin treatment suppressed the oxidative stress induced by acetaldehyde and restored the antioxidative capacity of SH-SY5Y cells. Therefore, astaxanthin may protect cells against acetaldehyde-induced cytotoxicity through maintaining redox balance and modulating apoptotic and survival signals. The results suggest that astaxanthin treatment may be beneficial for preventing neurotoxicity associated with acetaldehyde and excessive alcohol consumption. 相似文献
16.
Choo-Aun Neoh Robert Y.-L. Wang Zhong-Hao Din Jui-Hsin Su Yu-Kuei Chen Feng-Jen Tsai Shun-Hsiang Weng Yu-Jen Wu 《Marine drugs》2012,10(12):2893-2911
Sinulariolide, an isolated compound from the soft coral Sinularia flexibilis, possesses the anti-proliferative, anti-migratory and apoptosis-inducing activities against the TSGH bladder carcinoma cell. The anti-tumor effects of sinulariolide were determined by 3-(4,5-cimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay, cell migration assay and flow cytometry, respectively. Sinulariolide inhibited the growth and migration of bladder carcinoma cells in a dose-dependent manner, as well as induced both early and late apoptosis as determined by the flow cytometer. Also, the sinulariolide-induced apoptosis is related to the mitochondrial-mediated apoptosis via caspase-dependent pathways, elucidated by the loss of mitochondrial membrane potential, release of cytochrome C, activation of caspase-3/-9, Bax and Bad, as well as suppression of Bcl-2/Bcl-xL/Mcl-1. Detection of the PARP-1 cleaved product suggested the partial involvement of caspase-independent pathways. Moreover, inhibition of p38MAPK activity leads to the rescue of the cell cytotoxicity of sinulariolide-treated TSGH cells, indicating that the p38MAPK pathway is also involved in the sinulariolide-induced cell apoptosis. Altogether, these results suggest that sinulariolide induces apoptosis against bladder cancer cells through mitochondrial-related and p38MAPK pathways. 相似文献
17.
Soil cadmium (Cd) causes toxicity and oxidative stress, alters biochemical processes and rootknot formation in rice. Irrigation of exogenous peroxidase (POX) together with its co-substrate H2O2(POXRice + H2O2), is likely to have protective effect upon the biochemical and nodular changes in ricegrown in Cd-rich soil. Exposure to Cd concentration of 1.00 mg/L increased oxidative stress, loss of cellviability, electrolyte leakage and root knot formation, whereas it significantly lowered the chlorophyll leveland rhizobium growth in rice. Irrigation of exogenous POXRice + H2O2 to Cd-stressed rice seedlingsreversed the Cd-induced alterations in rice to levels similar in control (non-stressed) seedlings. Resultsprovided strong evidence of exogenous POXRice + H2O2-mediated reversal and restoration of physiologicaland biochemical processes as well as increased resistance of rice seedlings to root knot formation.Irrigation with POXRice + H2O2 appeared to contribute towards bringing normoxic conditions in the otherwisehypoxic soil environment by enhancing the O2 in pot-experiments due to reduced Cd uptake, enhancedmineral homeostasis of essential elements viz. P, Fe, Mo, Mg and Mn for maintenance of root architecturedamaged by lipid peroxidation and reduction in oxidative stress by reducing Cd-induced reactive oxygenspecies generation. Therefore, the mitigation of Cd-toxicity in rice through this novel approach appeared tobe a promising mode to limit Cd-uptake, modulate protective and tolerance mechanisms for sustainablerice yield in Cd-contaminated rice-croplands and prevent nematode attack in rice, however, more detailedstudies are needed prior to large scale applications. 相似文献
18.
外源腐胺对干旱胁迫下冬小麦幼苗叶片膜脂过氧化的调节效应 总被引：2，自引：0，他引：2
为了研究外源物质对小麦抗旱性的诱导作用,水培条件下研究了外源腐胺对干旱胁迫(15%PEG-6000)条件下冬小麦幼苗叶片膜脂过氧化及抗氧化酶活性的影响.结果表明,干旱胁迫48 h后冬小麦幼苗叶片含水量下降了27.43%, O_2(÷)的产生速率、丙二醛(MDA)和H_2O_2含量随时间的推移均呈增加的趋势,SOD、POD、CAT活性分别下降了23%、37%、70%.外源腐胺处理下叶片含水量仅下降了7.62%;叶片 MDA含量降低80%左右,H_2O_2的含量下降50%左右,O_2(÷)的产生速率降低了1/3,而叶片SOD、POD、CAT活性分别提高了41%、165.8%、246%.因此认为,外源腐胺可通过抑制活性氧(O_2,H_2O_2)的产生,降低MDA含量,提高抗氧化酶(SOD、POD、CAT)的活性,缓解干旱胁迫造成的冬小麦幼苗叶片细胞膜脂过氧化损伤,提高冬小麦的抗旱性. 相似文献
19.
Baiping Liu Yongping Zhang Zhiyou Yang Meijun Liu Cai Zhang Yuntao Zhao Cai Song 《Marine drugs》2021,19(11)
Microglia M1 phenotype causes HPA axis hyperactivity, neurotransmitter dysfunction, and production of proinflammatory mediators and oxidants, which may contribute to the etiology of depression and neurodegenerative diseases. Eicosapentaenoic acid (EPA) may counteract neuroinflammation by increasing n-3 docosapentaenoic acid (DPA). However, the cellular and molecular mechanisms of DPA, as well as whether it can exert antineuroinflammatory and neuroprotective effects, are unknown. The present study first evaluated DPA’s antineuroinflammatory effects in lipopolysaccharide (LPS)-activated BV2 microglia. The results showed that 50 μM DPA significantly decreased BV2 cell viability after 100 ng/mL LPS stimulation, which was associated with significant downregulation of microglia M1 phenotype markers and proinflammatory cytokines but upregulation of M2 markers and anti-inflammatory cytokine. Then, DPA inhibited the activation of mitogen-activated protein kinase (MAPK) p38 and nuclear factor-κB (NF-κB) p65 pathways, which results were similar to the effects of NF-κB inhibitor, a positive control. Second, BV2 cell supernatant was cultured with differentiated SH-SY5Y neurons. The results showed that the supernatant from LPS-activated BV2 cells significantly decreased SH-SY5Y cell viability and brain-derived neurotrophic factor (BDNF), TrkB, p-AKT, and PI3K expression, which were significantly reversed by DPA pretreatment. Furthermore, DPA neuroprotection was abrogated by BDNF-SiRNA. Therefore, n-3 DPA may protect neurons from neuroinflammation-induced damage by balancing microglia M1 and M2 polarizations, inhibiting microglia-NF-κB and MAPK p38 while activating neuron-BDNF/TrkB-PI3K/AKT pathways. 相似文献