Specifically, this study is designed to examine the possibility of TLR4 as a candidate receptor interacted with G. atrum polysaccharide (PSG-1) and elucidate the role of reactive oxygen species (ROS) in PSG-1-induced tumor necrosis factor-α (TNF-α) …

2017年12月21日 · Here, we show that palmitate-stimulated CD11b + F4/80 low hepatic infiltrating macrophages, but not CD11b + F4/80 high Kupffer cells, generate ROS via dynamin-mediated endocytosis of TLR4 and...

2014年4月1日 · Specifically, this study is designed to examine the possibility of TLR4 as a candidate receptor interacted with G. atrum polysaccharide (PSG-1) and elucidate the role of reactive oxygen species (ROS) in PSG-1-induced tumor necrosis factor-α (TNF-α) production during macrophage activation.

2020年5月21日 · We found that autophagy and ROS were required for S.pn -induced NETs formation. Moreover, TLR4 partly mediated NETs formation in response to S.pn in vitro and in vivo during AOM. We also showed...

2011年4月28日 · ECSIT- and TRAF6-depleted macrophages have decreased levels of TLR-induced ROS and are significantly impaired in their ability to kill intracellular bacteria. Additionally, reducing macrophage mROS levels by expressing catalase in mitochondria results in defective bacterial killing, confirming the role of mROS in bactericidal activity.

Using mice lacking a functional toll-like receptor 4 (TLR4), we demonstrate that TLR4 and ROS work in concert to mediate microglia activation, where the contribution from each pathway is dependent on the concentration of LPS.

2011年4月1日 · 在这里，我们证明了 Toll 样受体子集（TLR1、TLR2 和 TLR4）的参与导致线粒体募集到巨噬细胞吞噬体并增加 mROS 的产生。 这种反应涉及 TLR 信号转导子、肿瘤坏死因子受体相关因子 6 (TRAF6) 向线粒体的易位，它与蛋白质 ECSIT（Toll 通路中进化保守的信号中间体）结 …

ROS and RNS signaling were demonstrated to be related to TLR4-dependent NF-κB activation and inflammatory cytokines production (Weigert et al., 2018). The membrane-associated enzyme complex NADPH acts as a key intermediate in regulating the TLR4-mediated production of ROS.

2015年8月31日 · In the present study, we demonstrate that the TLR4- and TLR2-induced IRAK-ERK pathway cross-talks with p67phox-Nox-2 for ROS generation, thus regulating IL-1β transcription and processing in...

通过 N-乙酰半胱氨酸 (NAC) 治疗或敲除 SAP 小鼠中的 TLR4 可以改善脾脏 ROS 和线粒体功能障碍。 同时，我们发现NAC治疗还可以改善脾组织的自噬，提示脾脏ROS可能影响自噬受损，导致受损线粒体堆积，加重脾损伤。 此外，我们验证了脾损伤的机制是由脾 ROS 影响 PI3K/p-AKT/mTOR 通路介导的自噬引起的。 此外，我们发现SAP引起的脾损伤可以降低小鼠血清中促吞噬素的浓度。 然而，外源性补充促吞噬素可改善受损脾脏的病理损伤、ROS积累、自噬受损 …