共查询到19条相似文献,搜索用时 640 毫秒
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《动物营养学报》2021,33(6)
内质网是蛋白质在哺乳动物细胞内修饰、折叠和加工的场所。内质网的功能发生障碍时,未折叠蛋白或错误折叠蛋白在内质网腔中大量蓄积并激活内质网应激信号,细胞通过减少新蛋白质的合成或促进已合成蛋白质的折叠,恢复内质网稳态。因此,内质网应激信号是机体应对不利外界环境的适应性反应。严重的内质网应激可引发细胞凋亡,清除受损细胞。最近的研究发现,断奶仔猪肠道屏障功能障碍的发病过程伴随未折叠蛋白反应和内质网应激,合理的氨基酸营养可以通过调节内质网应激信号相关蛋白,恢复肠上皮屏障功能。本文对内质网应激影响猪肠道屏障功能的研究进展进行总结和综述,为通过营养物质调节内质网应激信号通路改善仔猪肠道健康提供参考。 相似文献
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内质网应激(endoplasmic reticulum stress, ERS)是细胞为应对内质网腔内错误折叠与未折叠蛋白聚集以及钙离子平衡紊乱等状况,而激活未折叠蛋白反应(unfolded protein response, UPR)、内质网过载反应和Caspase-12介导的凋亡通路等信号途径的反应过程,是细胞的一种保护性应激行为。ERS主要通过激活细胞内UPR,促进内质网正常功能的恢复。在病毒感染过程中,病毒会“劫持”细胞内质网合成大量病毒蛋白,加之细胞自身蛋白合成的需求,内质网中蛋白质合成超出了细胞的正常处理范围,造成大量未折叠或者错误折叠蛋白的积聚,接着诱导ERS和激活UPR。ERS作为细胞的一种保护性应激反应,在机体抗病毒感染和调节天然免疫反应中发挥着重要的作用。本研究对ERS的产生及功能、ERS与天然免疫信号通路的交互调控以及ERS诱导的细胞凋亡等方面进行了综述,以期为进一步研究抗病毒策略提供新思路。 相似文献
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陈宇郑彦楷李大彪邢媛媛 《动物营养学报》2023,(12):7641-7647
内质网是细胞内负责蛋白质折叠和修饰的重要细胞器。内质网应激是由于蛋白质异常累积而引起的细胞应激反应,可导致炎症、氧化损伤和细胞凋亡等动物机体的不良反应。近年来的研究表明,植物多糖可通过内质网应激介导的内质网过载反应和未折叠蛋白质反应相关通路,缓解内质网应激,进而保护动物机体免受损伤。本文综述了植物多糖在缓解内质网应激导致的动物机体炎症、氧化损伤和细胞凋亡等方面的相关机制和研究进展。 相似文献
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C/EBP同源蛋白CHOP是一种29K的细胞蛋白,主要参与调控细胞增殖、分化以及能量代谢等。CHOP作为转录因子在内质网应激(ER Stress,ERS)介导的细胞凋亡中起重要作用。ERS通常是指ER中错误折叠或未折叠蛋白质增加引起的应激反应。发生ERS时,细胞会通过未折叠蛋白反应(UPR)维持细胞内稳态。长期或过度的应激会导致ER功能障碍和凋亡发生。ER通过3个主要途径诱导细胞凋亡,包括IRE1/ASK1/JNK途径、Caspase-12 激酶途径和CHOP途径。 相似文献
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《动物医学进展》2020,(4)
在卵母细胞成熟过程中以及胚胎着床前,具备特定功能的各类蛋白质必须在内质网(endoplasmic reticulum,ER)中完成折叠与修饰,这对于维持卵母细胞成熟和胚胎发育是至关重要的。然而,外界不良因素的刺激会破坏内质网功能,阻碍蛋白质合成,诱发ER应激和未折叠蛋白反应(unfolded protein response,UPR),适当的应激反应有利于细胞恢复功能。卵母细胞和早期胚胎对各类外源刺激高度敏感,多项研究表明ER应激和UPR信号影响卵母细胞成熟和胚胎着床前发育。论文总结了ER应激、UPR信号通路及其在哺乳动物卵母细胞成熟和胚胎着床前发育中的作用和机制的现状,以期为卵母细胞体外发育成熟及人类生殖临床提供借鉴。 相似文献
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Molecular insights into the mechanisms of liver‐associated diseases in early‐lactating dairy cows: hypothetical role of endoplasmic reticulum stress 下载免费PDF全文
R. Ringseis D. K. Gessner K. Eder 《Journal of animal physiology and animal nutrition》2015,99(4):626-645
The transition period represents the most critical period in the productive life of high‐yielding dairy cows due to both metabolic and inflammatory stimuli, which challenge the liver and predispose dairy cows to develop liver‐associated diseases such as fatty liver and ketosis. Despite the fact that all high‐yielding dairy cows are affected by marked metabolic stress due to a severe negative energy balance (NEB) during early lactation, not all cows develop liver‐associated diseases. Although the reason for this is largely unknown, this indicates that the capacity of the liver to cope with metabolic and inflammatory challenges varies between individual high‐yielding dairy cows. Convincing evidence exists that endoplasmic reticulum (ER) stress plays a key role in the development of fatty liver, and it has been recently shown that ER stress occurs in the liver of high‐yielding dairy cows. This indicates that ER stress may be involved in the development of liver‐associated diseases in dairy cows. The present review shows that the liver of dairy cows during early lactation is exposed to several metabolic and inflammatory challenges, such as non‐esterified fatty acids, tumour necrosis factor α, interleukin‐1β, reactive oxygen species and lipopolysaccharides, which are known inducers of ER stress. Thus, ER stress may represent a molecular basis for fatty liver development and account for the frequent occurrence of fatty liver and ketosis in high‐yielding dairy cows. Interindividual differences between dairy cows in the activation of hepatic stress response pathways, such as nuclear factor E2‐related factor 2, which is activated during ER stress and reduces the sensitivity of tissues to oxidative and inflammatory damage, might provide an explanation at the molecular level for differences in the capacity to cope with pathological inflammatory challenges during early lactation and the susceptibility to develop liver‐associated diseases between early‐lactating dairy cows with similar NEB and milk yield. 相似文献
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Ruonan Li Yu Yang Pan Hong Ziqi Zhang Lingqian Li Junnan Hui Xin Zheng 《Journal of animal physiology and animal nutrition》2020,104(1):280-290
Weaning may cause oxidative injury, immune response impairment, apoptosis and other injuries in piglets. Oxidative and endoplasmic reticulum stress (ERS) can elicit inflammatory responses, and persistent oxidative and ERS also may lead to apoptotic cascades, which is associated with the pathogenesis of multiple diseases. β-carotene, a natural carotenoid, has potential anti-inflammatory and antioxidant functions. However, the effect of β-carotene on apoptosis in weaned piglets and the detailed molecular mechanism remain unclear. In this study, we found that β-carotene decreased malondialdehyde (MDA) levels and increased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in piglet serum. β-carotene could inhibit the mRNA levels of caspase-3 significantly, but had no significant inhibitory effect of the mRNA levels of caspase-9 and caspase-12 in the piglet jejunum. In addition, β-carotene decreased the activation of GRP78, CHOP, and JNK/p38 MAPK and the ratio of Bax/Bcl-2. Furthermore, β-carotene had a significant influence on the activation of ERS and apoptosis-related signals in TG-induced IPEC-J2. In the present study, β-carotene pre-treatment attenuated the ratio of Bax/Bcl-2 and prevented TG-induced increases in the level of PERK-CHOP and IRE1-JNK/p38 MAPK pathway activation in a dose-dependent manner. Overall, these findings indicate that β-carotene may protect weaning-induced apoptosis through inhibiting ERS. 相似文献
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【目的】探讨伪狂犬病毒(PRV)感染对BHK-21悬浮细胞内质网应激及未折叠蛋白反应(UPR)的影响。【方法】将悬浮的乳仓鼠肾细胞(BHK-21)以感染复数(MOI)0.01接种PRV,分别在接毒后12、24、36、48和56 h取样,用CCK-8法检测细胞存活率,按Reed-Muench法检测病毒滴度,筛选病毒接种处理的合适时间;以不接毒细胞作对照组,分别在感染后12、24、36和48 h取样,用实时荧光定量PCR法检测内质网应激标志分子葡萄糖调节蛋白78(GRP78)及UPR的3种感受蛋白(PERK、IRE1、ATF6)相关通路中基因的表达变化,Western blotting法检测相关蛋白的表达变化。在接种PRV同时分别加入0、0.001、0.005、0.01和0.02 μmol/L内质网应激诱导剂毒胡萝卜素(Tg)和0、20、40、80和160 μmol/L内质网应激抑制剂牛磺熊去氧胆酸(TUDCA),48 h收集细胞测定病毒滴度和细胞存活率。【结果】PRV感染56 h细胞存活率低于70%,感染48 h时病毒滴度达到最高(8.1 lg TCID50/mL),因此后续试验分别在接毒后12、24、36和48 h取样。与对照组相比,PRV感染36和48 h GRP78转录水平均极显著升高(P<0.01);PERK通路中,转录激活因子4(ATF4)转录水平在PRV感染36、48 h均极显著升高(P<0.01),生长抑制DNA损伤基因34(GADD34)转录水平在PRV感染36 h显著升高(P<0.05)、48 h极显著升高(P<0.01),磷酸化真核翻译起始因子(P-eIF2α)蛋白水平在PRV感染36、48 h均极显著升高(P<0.01);IRE1通路中,PRV感染组细胞36 h后多以剪切形式sXBP1存在,同时下游p58IPKmRNA水平在36 h显著增加(P<0.05),p58IPK和EDEM mRNA水平在48 h均极显著增加(P<0.01);ATF6通路中,PRV感染不同时间ERp57、PDI、Calnexin和Calreticulin的表达均无显著变化(P>0.05)。与0 μmol/L组相比,0.01和0.02 μmol/L Tg极显著降低细胞存活率(P<0.01),0.005和0.01 μmol/L Tg均极显著增加了PRV病毒滴度(P<0.01)。【结论】PRV感染可以诱导BHK-21悬浮细胞内质网应激,激活UPR的PERK和IRE1信号通路,说明PRV利用内质网应激增强其复制。 相似文献
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