Suppressing mPGES-1 expression by sinomenine ameliorates inflammation and arthritis

Hua Zhou; Jian Xin Liu; Jin Fang Luo; Chun Song Cheng; Elaine Lai Han Leung; Ying Li; Xiao Hui Su; Zhong Qiu Liu; Ting Bo Chen; Fu Gang Duan; Yan Dong; Yi Han Zuo; Chong Li; Chon Kit Lio; Ting Li; Pei Luo; Ying Xie; Xiao Jun Yao; Pei Xun Wang; Liang Liu

doi:10.1016/j.bcp.2017.07.010

Suppressing mPGES-1 expression by sinomenine ameliorates inflammation and arthritis

Hua Zhou, Jian Xin Liu, Jin Fang Luo, Chun Song Cheng, Elaine Lai Han Leung, Ying Li, Xiao Hui Su, Zhong Qiu Liu, Ting Bo Chen, Fu Gang Duan, Yan Dong, Yi Han Zuo, Chong Li, Chon Kit Lio, Ting Li, Pei Luo, Ying Xie, Xiao Jun Yao, Pei Xun Wang, Liang Liu

Research output: Contribution to journal › Article › peer-review

58 Scopus citations

Abstract

Recently, microsomal prostaglandin E synthase 1 (mPGES-1) has attracted much attention from pharmacologists as a promising strategy and an attractive target for treating various types of diseases including rheumatoid arthritis (RA), which could preserve the anti-inflammatory effect while reducing the adverse effects often occur during administration of non-steroidal anti-inflammatory drugs (NSAIDs). Here, we report that sinomenine (SIN) decreased prostaglandin (PG)E₂ levels without affecting prostacyclin (PG)I₂ and thromboxane (TX)A₂ synthesis via selective inhibiting mPGES-1 expression, a possible reason of low risk of cardiovascular event compared with NSAIDs. In addition, mPGES-1 protein expression was down-regulated by SIN treatment in the inflamed paw tissues both in carrageenan-induced edema model in rats and the collagen-II induced arthritis (CIA) model in DBA mice. More interestingly, SIN suppressed the last step of mPGES-1 gene expression by decreasing the DNA binding ability of NF-κB, paving a new way for drug discovery.

Original language	English (US)
Pages (from-to)	133-144
Number of pages	12
Journal	Biochemical Pharmacology
Volume	142
DOIs	https://doi.org/10.1016/j.bcp.2017.07.010
State	Published - Oct 15 2017
Externally published	Yes

Keywords

Inflammation
NF-κB
Rheumatoid arthritis
Sinomenine
mPGES-1

ASJC Scopus subject areas

Biochemistry
Pharmacology

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10.1016/j.bcp.2017.07.010

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Zhou, H., Liu, J. X., Luo, J. F., Cheng, C. S., Leung, E. L. H., Li, Y., Su, X. H., Liu, Z. Q., Chen, T. B., Duan, F. G., Dong, Y., Zuo, Y. H., Li, C., Lio, C. K., Li, T., Luo, P., Xie, Y., Yao, X. J., Wang, P. X., & Liu, L. (2017). Suppressing mPGES-1 expression by sinomenine ameliorates inflammation and arthritis. Biochemical Pharmacology, 142, 133-144. https://doi.org/10.1016/j.bcp.2017.07.010

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title = "Suppressing mPGES-1 expression by sinomenine ameliorates inflammation and arthritis",

abstract = "Recently, microsomal prostaglandin E synthase 1 (mPGES-1) has attracted much attention from pharmacologists as a promising strategy and an attractive target for treating various types of diseases including rheumatoid arthritis (RA), which could preserve the anti-inflammatory effect while reducing the adverse effects often occur during administration of non-steroidal anti-inflammatory drugs (NSAIDs). Here, we report that sinomenine (SIN) decreased prostaglandin (PG)E2 levels without affecting prostacyclin (PG)I2 and thromboxane (TX)A2 synthesis via selective inhibiting mPGES-1 expression, a possible reason of low risk of cardiovascular event compared with NSAIDs. In addition, mPGES-1 protein expression was down-regulated by SIN treatment in the inflamed paw tissues both in carrageenan-induced edema model in rats and the collagen-II induced arthritis (CIA) model in DBA mice. More interestingly, SIN suppressed the last step of mPGES-1 gene expression by decreasing the DNA binding ability of NF-κB, paving a new way for drug discovery.",

keywords = "Inflammation, NF-κB, Rheumatoid arthritis, Sinomenine, mPGES-1",

author = "Hua Zhou and Liu, {Jian Xin} and Luo, {Jin Fang} and Cheng, {Chun Song} and Leung, {Elaine Lai Han} and Ying Li and Su, {Xiao Hui} and Liu, {Zhong Qiu} and Chen, {Ting Bo} and Duan, {Fu Gang} and Yan Dong and Zuo, {Yi Han} and Chong Li and Lio, {Chon Kit} and Ting Li and Pei Luo and Ying Xie and Yao, {Xiao Jun} and Wang, {Pei Xun} and Liang Liu",

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AU - Zhou, Hua

AU - Liu, Jian Xin

AU - Luo, Jin Fang

AU - Cheng, Chun Song

AU - Leung, Elaine Lai Han

AU - Li, Ying

AU - Su, Xiao Hui

AU - Liu, Zhong Qiu

AU - Chen, Ting Bo

AU - Duan, Fu Gang

AU - Dong, Yan

AU - Zuo, Yi Han

AU - Li, Chong

AU - Lio, Chon Kit

AU - Li, Ting

AU - Luo, Pei

AU - Xie, Ying

AU - Yao, Xiao Jun

AU - Wang, Pei Xun

AU - Liu, Liang

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N2 - Recently, microsomal prostaglandin E synthase 1 (mPGES-1) has attracted much attention from pharmacologists as a promising strategy and an attractive target for treating various types of diseases including rheumatoid arthritis (RA), which could preserve the anti-inflammatory effect while reducing the adverse effects often occur during administration of non-steroidal anti-inflammatory drugs (NSAIDs). Here, we report that sinomenine (SIN) decreased prostaglandin (PG)E2 levels without affecting prostacyclin (PG)I2 and thromboxane (TX)A2 synthesis via selective inhibiting mPGES-1 expression, a possible reason of low risk of cardiovascular event compared with NSAIDs. In addition, mPGES-1 protein expression was down-regulated by SIN treatment in the inflamed paw tissues both in carrageenan-induced edema model in rats and the collagen-II induced arthritis (CIA) model in DBA mice. More interestingly, SIN suppressed the last step of mPGES-1 gene expression by decreasing the DNA binding ability of NF-κB, paving a new way for drug discovery.

AB - Recently, microsomal prostaglandin E synthase 1 (mPGES-1) has attracted much attention from pharmacologists as a promising strategy and an attractive target for treating various types of diseases including rheumatoid arthritis (RA), which could preserve the anti-inflammatory effect while reducing the adverse effects often occur during administration of non-steroidal anti-inflammatory drugs (NSAIDs). Here, we report that sinomenine (SIN) decreased prostaglandin (PG)E2 levels without affecting prostacyclin (PG)I2 and thromboxane (TX)A2 synthesis via selective inhibiting mPGES-1 expression, a possible reason of low risk of cardiovascular event compared with NSAIDs. In addition, mPGES-1 protein expression was down-regulated by SIN treatment in the inflamed paw tissues both in carrageenan-induced edema model in rats and the collagen-II induced arthritis (CIA) model in DBA mice. More interestingly, SIN suppressed the last step of mPGES-1 gene expression by decreasing the DNA binding ability of NF-κB, paving a new way for drug discovery.

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Suppressing mPGES-1 expression by sinomenine ameliorates inflammation and arthritis

Abstract

Keywords

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