Novel chimeric TLR2/NOD2 agonist CL429 exhibited significant radioprotective effects in mice.
Novel chimeric TLR2/NOD2 agonist CL429 exhibited significant radioprotective effects in mice.
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新型嵌合TLR2/NOD2激动剂CL429在小鼠中表现出显着的辐射防护作用
DOI：
10.1111/jcmm.16252
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发表时间：
2021-04
影响因子：
5.3
通讯作者：
Liu C
中科院分区：
文献类型：
--
作者：
Cheng Y;Du J;Liu R;Dong S;Cai J;Gao F;Liu C
严重的电离辐射会对造血系统和胃肠道造成急性致命性损害。在这里，我们发现新型嵌合TLR2/NOD2激动剂CL429在小鼠身上显示出显著的辐射防护作用。CL429可提高小鼠存活率，保护小鼠免受造血系统和胃肠道的致死性损伤。CL429比等量的单特异性分子(TLR2或NOD2)和组合(TLR2+NOD2)更有效地预防辐射诱导的死亡。CL429的辐射防护作用主要是通过激活TLR2和部分激活NOD2实现的。Cl429诱导的辐射防护很大程度上依赖于TLR2-MyD88-NF-κB信号通路的激活。综上所述，TLR2和NOD2的共激活可以诱导出显著的协同辐射防护效应，CL429可能是一种潜在的高效选择剂。
Severe ionizing radiation causes the acute lethal damage of haematopoietic system and gastrointestinal tract. Here, we found CL429, the novel chimeric TLR2/NOD2 agonist, exhibited significant radioprotective effects in mice. CL429 increased mice survival, protected mice against the lethal damage of haematopoietic system and gastrointestinal tract. CL429 was more effective than equivalent amounts of monospecific (TLR2 or NOD2) and combination (TLR2 + NOD2) of molecules in preventing radiation‐induced death. The radioprotection of CL429 was mainly mediated by activating TLR2 and partially activating NOD2. CL429‐induced radioprotection was largely dependent on the activation of TLR2‐MyD88‐NF‐κB signalling pathway. In conclusion, the data suggested that the co‐activation of TLR2 and NOD2 could induce significant synergistic radioprotective effects and CL429 might be a potential high‐efficiency selective agent.
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DOI：
10.1126/science.aaf7532
发表时间：
2016-11-11
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Hu B;Jin C;Li HB;Tong J;Ouyang X;Cetinbas NM;Zhu S;Strowig T;Lam FC;Zhao C;Henao-Mejia J;Yilmaz O;Fitzgerald KA;Eisenbarth SC;Elinav E;Flavell RA
通讯作者：
Flavell RA
影响因子：
29.7
作者：
Brubaker SW;Bonham KS;Zanoni I;Kagan JC
通讯作者：
Kagan JC
影响因子：
2.6
作者：
Chen, Yangbin
通讯作者：
Chen, Yangbin
影响因子：
16.6
作者：
Takemura, Naoki;Kawasaki, Takumi;Kunisawa, Jun;Sato, Shintaro;Lamichhane, Aayam;Kobiyama, Kouji;Aoshi, Taiki;Ito, Junichi;Mizuguchi, Kenji;Karuppuchamy, Thangaraj;Matsunaga, Kouta;Miyatake, Shoichiro;Mori, Nobuko;Tsujimura, Tohru;Satoh, Takashi;Kumagai, Yutaro;Kawai, Taro;Standley, Daron M.;Ishii, Ken J.;Kiyono, Hiroshi;Akira, Shizuo;Uematsu, Satoshi
通讯作者：
Uematsu, Satoshi
影响因子：
29.7
作者：
Caballero S;Pamer EG
通讯作者：
Pamer EG