Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
Kaiwen W Chen, Benjamin Demarco, Petr Bro. Pannexin-1 promotes NLRP3 activation during apoptosis but is dispensable for canonical or noncanonical inflammasome activation. European journal of immunology. vol 50. issue 2. 2020-07-13. PMID:31411729. |
pannexin-1 promotes nlrp3 activation during apoptosis but is dispensable for canonical or noncanonical inflammasome activation. |
2020-07-13 |
2023-08-13 |
Not clear |
Kaiwen W Chen, Benjamin Demarco, Petr Bro. Pannexin-1 promotes NLRP3 activation during apoptosis but is dispensable for canonical or noncanonical inflammasome activation. European journal of immunology. vol 50. issue 2. 2020-07-13. PMID:31411729. |
pannexin-1 is channel-forming glycoprotein that promotes membrane permeability and atp release during apoptosis; and was implicated in canonical nlrp3 or noncanonical inflammasome activation. |
2020-07-13 |
2023-08-13 |
Not clear |
Yang Gyun Kim, Su-Mi Kim, Ki-Pyo Kim, Sang-Ho Lee, Ju-Young Moo. The Role of Inflammasome-Dependent and Inflammasome-Independent NLRP3 in the Kidney. Cells. vol 8. issue 11. 2020-07-08. PMID:31694192. |
inflammasome-independent nlrp3 regulates apoptosis in tubular epithelial cells by interacting with mitochondria and mediating mitochondrial reactive oxygen species production and mitophagy. |
2020-07-08 |
2023-08-13 |
Not clear |
Guanwen Huang, Jiwen Bao, Xinghua Shao, Wenyan Zhou, Bei Wu, Zhaohui Ni, Ling Wan. Inhibiting pannexin-1 alleviates sepsis-induced acute kidney injury via decreasing NLRP3 inflammasome activation and cell apoptosis. Life sciences. vol 254. 2020-06-29. PMID:32416166. |
inhibiting pannexin-1 alleviates sepsis-induced acute kidney injury via decreasing nlrp3 inflammasome activation and cell apoptosis. |
2020-06-29 |
2023-08-13 |
Not clear |
Jun Li, Sha-Sha Zuo, Xiao-Xuan Qiu, Xi Xu, Ying-Ying Luo, Hong-Wei Gao, Yu-Lin Feng, Li-Jun DU, Qin Gon. [Expression characteristics of inflammatory and apoptosis factors and regulatory effect of anemoside B4 in mice with acute kidney injury]. Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica. vol 45. issue 1. 2020-06-25. PMID:32237425. |
after the serum was separated, serum urea nitrogen(bun), creatinine(cre), total protein(tp), and albumin(alb) were tested by using an automatic biochemical analyzer; the changes of kidney pathological morphology were observed by pas staining; the protein expression levels of inflammatory factors including nucleotide binding oligomerization domain-like receptor(nlrp3), cysteinyl aspartate specific proteinase 1(caspase-1), interleukin-18(il-18), interleukin-1β(il-1β), tumor necrosis factor(tnf-α), and interleukin-6(il-6) and apoptosis factors including p53, caspase-3, cleaved-caspase-3, bcl-2 associated x protein(bax), and b-cell lymphoma-2(bcl-2) were analyzed by western blot. |
2020-06-25 |
2023-08-13 |
mouse |
Qiang Sun, Songlin Wang, Jun Chen, Hongxia Cai, Wei Huang, Yueliang Zhang, Lei Wang, Yu Xin. MicroRNA-190 alleviates neuronal damage and inhibits neuroinflammation via Nlrp3 in MPTP-induced Parkinson's disease mouse model. Journal of cellular physiology. vol 234. issue 12. 2020-06-08. PMID:31232472. |
furthermore, upregulation of mir-190 or knockdown of nlrp3 inhibited lps-induced apoptosis in bv2 cells. |
2020-06-08 |
2023-08-13 |
mouse |
Qiang Sun, Songlin Wang, Jun Chen, Hongxia Cai, Wei Huang, Yueliang Zhang, Lei Wang, Yu Xin. MicroRNA-190 alleviates neuronal damage and inhibits neuroinflammation via Nlrp3 in MPTP-induced Parkinson's disease mouse model. Journal of cellular physiology. vol 234. issue 12. 2020-06-08. PMID:31232472. |
however, the apoptosis inhibition effect of mir-190 was abrogated by overexpression of nlrp3. |
2020-06-08 |
2023-08-13 |
mouse |
Zhenen Zhang, Nannan Han, Ye She. S100A12 promotes inflammation and cell apoptosis in sepsis-induced ARDS via activation of NLRP3 inflammasome signaling. Molecular immunology. vol 122. 2020-06-08. PMID:32298873. |
s100a12 promotes inflammation and cell apoptosis in sepsis-induced ards via activation of nlrp3 inflammasome signaling. |
2020-06-08 |
2023-08-13 |
mouse |
Maki Inoue, Toshinori Okinaga, Michihiko Usui, Aki Kawano, Chuencheewit Thongsiri, Keisuke Nakashima, Wataru Ariyoshi, Tatsuji Nishihar. β-glucan suppresses cell death of ASC deficient macrophages invaded by periodontopathic bacteria through the caspase-11 pathway. FEMS microbiology letters. vol 366. issue 8. 2020-06-03. PMID:31098636. |
members of the nucleotide-binding domain leucine-rich repeat-containing (nlr) protein family, such as nlr protein 3 (nlrp3), nlr family apoptosis inhibitory protein (naip), and nlr family card domain-containing protein 4 (nlrc4), as well as an associated protein, caspase-11, were clearly detected in a. actinomycetemcomitans-invaded control raw cells (c-raw cells; negative control). |
2020-06-03 |
2023-08-13 |
mouse |
Wu Jiang, Maoqiang Li, Fan He, Liulong Zh. Inhibition of NLRP3 inflammasome attenuates spinal cord injury-induced lung injury in mice. Journal of cellular physiology. vol 234. issue 5. 2020-03-30. PMID:30589073. |
hence, it is inescapable to explore the effect of inhibition of nlrp3 inflammasome by inhibitors in a mouse sci model, which was conducted by using the method of 30-g closing force aneurysm clipping at t6-t7 spinal segment for 1 min, followed by assessment of edema, histology, alveolar type ii cell apoptosis, mitochondrial dysfunction, and neutrophil infiltration. |
2020-03-30 |
2023-08-13 |
mouse |
Wu Jiang, Maoqiang Li, Fan He, Liulong Zh. Inhibition of NLRP3 inflammasome attenuates spinal cord injury-induced lung injury in mice. Journal of cellular physiology. vol 234. issue 5. 2020-03-30. PMID:30589073. |
in brief, our results showed that, nlrp3 inflammasome inhibitor bay 11-7082 or a438079 inhibited activation of nlrp3 inflammasome, alleviated mitochondrial dysfunction, the number of macrophage and neutrophil, thereby attenuating alveolar type ii cell apoptosis, lung edema, and histological injury. |
2020-03-30 |
2023-08-13 |
mouse |
Jiezhi Dai, Hua Chen, Yimin Cha. Advanced Glycation End Products (AGEs) Induce Apoptosis of Fibroblasts by Activation of NLRP3 Inflammasome via Reactive Oxygen Species (ROS) Signaling Pathway. Medical science monitor : international medical journal of experimental and clinical research. vol 25. 2020-03-09. PMID:31587010. |
advanced glycation end products (ages) induce apoptosis of fibroblasts by activation of nlrp3 inflammasome via reactive oxygen species (ros) signaling pathway. |
2020-03-09 |
2023-08-13 |
human |
Jiezhi Dai, Hua Chen, Yimin Cha. Advanced Glycation End Products (AGEs) Induce Apoptosis of Fibroblasts by Activation of NLRP3 Inflammasome via Reactive Oxygen Species (ROS) Signaling Pathway. Medical science monitor : international medical journal of experimental and clinical research. vol 25. 2020-03-09. PMID:31587010. |
human dermal fibroblasts exposed to ages were used to study the links among apoptosis, ros, and nlrp3 inflammasome activation. |
2020-03-09 |
2023-08-13 |
human |
Jiezhi Dai, Hua Chen, Yimin Cha. Advanced Glycation End Products (AGEs) Induce Apoptosis of Fibroblasts by Activation of NLRP3 Inflammasome via Reactive Oxygen Species (ROS) Signaling Pathway. Medical science monitor : international medical journal of experimental and clinical research. vol 25. 2020-03-09. PMID:31587010. |
ages-induced apoptosis was blocked by bay 11-7082, an inhibitor of the nlrp3 inflammasome. |
2020-03-09 |
2023-08-13 |
human |
Jiezhi Dai, Hua Chen, Yimin Cha. Advanced Glycation End Products (AGEs) Induce Apoptosis of Fibroblasts by Activation of NLRP3 Inflammasome via Reactive Oxygen Species (ROS) Signaling Pathway. Medical science monitor : international medical journal of experimental and clinical research. vol 25. 2020-03-09. PMID:31587010. |
conclusions ages cause apoptosis of fibroblasts by inducing the generation of ros and activating the nlrp3 inflammasome. |
2020-03-09 |
2023-08-13 |
human |
Ning Li, Heng Zhou, Haiming Wu, Qingqing Wu, Mingxia Duan, Wei Deng, Qizhu Tan. STING-IRF3 contributes to lipopolysaccharide-induced cardiac dysfunction, inflammation, apoptosis and pyroptosis by activating NLRP3. Redox biology. vol 24. 2020-03-03. PMID:31121492. |
sting-irf3 contributes to lipopolysaccharide-induced cardiac dysfunction, inflammation, apoptosis and pyroptosis by activating nlrp3. |
2020-03-03 |
2023-08-13 |
mouse |
Qisheng Lin, Shu Li, Na Jiang, Xinghua Shao, Minfang Zhang, Haijiao Jin, Zhen Zhang, Jianxiao Shen, Yijun Zhou, Wenyan Zhou, Leyi Gu, Renhua Lu, Zhaohui N. PINK1-parkin pathway of mitophagy protects against contrast-induced acute kidney injury via decreasing mitochondrial ROS and NLRP3 inflammasome activation. Redox biology. vol 26. 2020-02-28. PMID:31229841. |
functionally, pink1-parkin-mediated mitophagy prevented rtec apoptosis and tissue damage in ci-aki through reducing mitochondrial ros and subsequent nlrp3 inflammasome activation. |
2020-02-28 |
2023-08-13 |
mouse |
Takanori Komada, Daniel A Muruv. The role of inflammasomes in kidney disease. Nature reviews. Nephrology. vol 15. issue 8. 2020-02-17. PMID:31164720. |
in particular, the nlrp3 (nod-, lrr- and pyrin domain-containing 3) inflammasome has been shown to contribute to a wide range of acute and chronic microbial and non-microbial kidney diseases via canonical and non-canonical mechanisms that regulate inflammation, pyroptosis, apoptosis and fibrosis. |
2020-02-17 |
2023-08-13 |
Not clear |
Hai-Chao Dong, Pei-Nan Li, Chang-Jian Chen, Xin Xu, Hong Zhang, Gang Liu, Lian-Jie Zheng, Peng L. Sinomenine Attenuates Cartilage Degeneration by Regulating miR-223-3p/NLRP3 Inflammasome Signaling. Inflammation. vol 42. issue 4. 2020-01-13. PMID:30847744. |
in vitro, we found that nlrp3 was a direct target of mir-223-3p, and overexpression of mir-223-3p blocked il-1β-induced apoptosis and the inflammatory response in chondrocytes. |
2020-01-13 |
2023-08-13 |
mouse |
Seung-Ju Yang, A Reum Han, Eun-A Kim, Ji Woong Yang, Jee-Yin Ahn, Jung-Min Na, Sung-Woo Ch. KHG21834 attenuates glutamate-induced mitochondrial damage, apoptosis, and NLRP3 inflammasome activation in SH-SY5Y human neuroblastoma cells. European journal of pharmacology. vol 856. 2020-01-13. PMID:31129157. |
khg21834 attenuates glutamate-induced mitochondrial damage, apoptosis, and nlrp3 inflammasome activation in sh-sy5y human neuroblastoma cells. |
2020-01-13 |
2023-08-13 |
human |