Schisandrin B protects against LPS-induced inflammatory lung injury by targeting MyD88

被引:19
|
作者
Zhu, Weiwei [1 ,2 ,3 ]
Luo, Wu [4 ]
Han, Jibo [1 ]
Zhang, Qiuyan [1 ]
Ji, Lijun [1 ,2 ]
Samorodov, Aleksandr V. [5 ]
Pavlov, Valentin N. [5 ]
Zhuang, Zaishou [6 ]
Yang, Daona [6 ]
Yin, Lina [7 ]
Huang, Lijiang [3 ]
Liang, Guang [6 ]
Huh, Joo Young [1 ,2 ]
Wang, Yi [1 ,2 ,3 ]
机构
[1] Wenzhou Med Univ, Chem Biol Res Ctr, Sch Pharmaceut Sci, Wenzhou 325035, Zhejiang, Peoples R China
[2] Chonnam Natl Univ, Coll Pharm, Gwangju 61186, South Korea
[3] Wenzhou Medial Univ, Affiliated Xiangshan Hosp, Xiangshan Peoples Hosp Med & Hlth Grp 1, Xiangshan 315799, Zhejiang, Peoples R China
[4] Wenzhou Med Univ, Affiliated Hosp 1, Med Res Ctr, Wenzhou 325000, Zhejiang, Peoples R China
[5] Bashkir State Med Univ, Dept Pharmacol, Ufa 450005, Russia
[6] Wenzhou Med Univ, Affiliated Cangnan Hosp, Cangnan 325800, Zhejiang, Peoples R China
[7] Hangzhou Med Coll, Sch Pharmaceut Sci, Hangzhou 311399, Zhejiang, Peoples R China
基金
中国国家自然科学基金;
关键词
Schisandrin B; MyD88; TLR4; Inflammation; Acute lung injury; NF-kappa B; CHINENSIS; RESPONSES;
D O I
10.1016/j.phymed.2022.154489
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Background: Acute lung injury (ALI) is a challenging clinical syndrome that manifests as an acute inflammatory response. Schisandrin B (Sch B), a bioactive lignan from Schisandra genus plants, has been shown to suppress inflammatory responses and oxidative stress. However, the underlying molecular mechanisms have remained elusive. Hypothesis/purpose: This study performed an in-depth investigation of the anti-inflammatory mechanism of Sch B in macrophages and in an animal model of ALI. Methods: qPCR array was used to probe the differential effects and potential target of Sch B. ALI was induced by intratracheal administration of LPS in experimental mice with or without Sch B treatment. Results: Our studies show that Sch B differentially modulates inflammatory factor induction by LPS in macro-phages by directly binding myeloid differentiation response factor-88 (MyD88), an essential adaptor protein in the toll-like receptor-4 (TLR4) pathway. Sch B spares non-MyD88-pathways downstream of TLR4. Such inhibi-tion suppressed key signaling mediators such as TAK1, MAPKs, and NF-kappa B, and pro-inflammatory factor in-duction. Pull down assay using biotinylated-Sch B validate the direct interaction between Sch B and MyD88 in macrophages. Treatment of mice with Sch B prior to LPS challenge reduced inflammatory cell infiltration in lungs, induction of MyD88-pathway signaling proteins, and prevented inflammatory cytokine induction. Conclusion: In summary, our studies have identified MyD88 as a direct target of Sch B for its anti-inflammatory activity, and suggest that Sch B may have therapeutic value for acute lung injury and other MyD88-dependent inflammatory diseases.
引用
收藏
页数:12
相关论文
共 50 条
  • [21] MyD88 plays a key role in LPS-induced Stat3 activation in the hypothalamus
    Yamawaki, Yosuke
    Kimura, Hitomi
    Hosoi, Toru
    Ozawa, Koichiro
    AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 2010, 298 (02) : R403 - R410
  • [22] Guben Tongluo Formula Protects LPS-induced Damage in Lamina Propria B Lymphocytes Through TLR4/MyD88/NF-κB Pathway
    Wu, Qing
    Meng, Wei
    Shen, Jiao-Jiao
    Bai, Jia-Yuan
    Wang, Luo-Bing
    Liang, Ting-Yu
    Huang, Di
    Shen, Pei-Cheng
    CURRENT MEDICAL SCIENCE, 2022, 42 (05) : 991 - 999
  • [23] Dexmedetomidine protects against lung injury induced by limb ischemia-reperfusion via the TLR4/MyD88/NF-κB pathway
    Xue, Bin-Bin
    Chen, Bai-Hui
    Tang, Ya-Ning
    Weng, Cheng-Wei
    Lin, Li-Na
    KAOHSIUNG JOURNAL OF MEDICAL SCIENCES, 2019, 35 (11): : 672 - 678
  • [24] Guben Tongluo Formula Protects LPS-induced Damage in Lamina Propria B Lymphocytes Through TLR4/MyD88/NF-κB Pathway
    Qing Wu
    Wei Meng
    Jiao-jiao Shen
    Jia-yuan Bai
    Luo-bing Wang
    Ting-yu Liang
    Di Huang
    Pei-cheng Shen
    Current Medical Science, 2022, 42 : 991 - 999
  • [25] Limonin, a novel AMPK activator, protects against LPS-induced acute lung injury
    Liang, Hui
    Liu, Gaoli
    Fan, Qinglu
    Nie, Zhihao
    Xie, Songping
    Zhang, Renquan
    INTERNATIONAL IMMUNOPHARMACOLOGY, 2023, 122
  • [26] MyD88 as a therapeutic target for inflammatory lung diseases
    Di Padova, Franco
    Quesniaux, Valerie F. J.
    Ryffel, Bernhard
    EXPERT OPINION ON THERAPEUTIC TARGETS, 2018, 22 (05) : 401 - 408
  • [27] Myd88 Signaling Is Involved in the Inflammatory Response in LPS-Induced Mouse Epididymitis and Bone-Marrow-Derived Dendritic Cells
    Liu, Jin-Chuan
    Wang, Peng
    Zeng, Qun-Xiong
    Yang, Chen
    Lyu, Minmin
    Li, Yanfeng
    Yeung, William Shu-Biu
    Chiu, Philip Chi-Ngong
    Haidl, Gerhard
    Allam, Jean-Pierre
    Duan, Yong-Gang
    INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2023, 24 (09)
  • [28] Stevioside Protects LPS-Induced Acute Lung Injury in Mice
    Nie Yingkun
    Wang Zhenyu
    Lin Jing
    Lu Xiuyun
    Yu Huimin
    Inflammation, 2013, 36 : 242 - 250
  • [29] Stevioside Protects LPS-Induced Acute Lung Injury in Mice
    Nie Yingkun
    Wang Zhenyu
    Lin Jing
    Lu Xiuyun
    Yu Huimin
    INFLAMMATION, 2013, 36 (01) : 242 - 250
  • [30] Shensongyangxin protects cardiomyocytes against LPS-induced injury through the NFκB pathway
    Shen, Di-Fei
    Ni, Jian
    Wu, Qing-Qing
    Deng, Wei
    Wei, Cong
    Jia, Zhen-Hua
    Zhou, Heng
    Zhou, Meng-Qiao
    Bian, Zhou-Yan
    Tang, Qi-Zhu
    INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE, 2016, 9 (02): : 2317 - 2324