The Journal of pharmacy and pharmacology · 2021
Chlorogenic acid ameliorates mice clinical endometritis by activating Keap1/Nrf2 and inhibiting NFκB signalling pathway.
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Gao Feng, Fu Kaiqiang, Li Huatao, Feng Yanni, Tian Wenru, Cao Rongfeng
Аннотация
OBJECTIVES: Clinical endometritis is a common reproductive disorder in mammals that seriously endangers animal health and causes economic losses worldwide. This study aims to use lipopolysaccharide and Trueperella pyogenes exotoxin as modelling reagents (LC) to perfuse the mouse uterus in order to establish a model of clinical endometritis and to investigate the anti-inflammatory and antioxidant effects of chlorogenic acid (CGA).
METHODS: In this study, five LC uterine perfusions were selected to model clinical endometritis. The anti-inflammatory and antioxidant effects of CGA were clarified. Through HE staining, proinflammatory cytokines, blood testing, NFκB and Keap1/Nrf2 signalling pathways and other index changes to explore the protection mechanism of CGA.
KEY FINDINGS: After CGA treatment, the appearance, inflammatory damage and blood indicators of the mouse uterus returned to normal. Simultaneously, CGA could inhibit the activation of NFκB and reduce the release of inflammatory cytokines; CGA could also activate Keap1/Nrf2, promote the dissociation of Keap1 and Nrf2 and significantly increase the expression of the downstream genes HO-1 and NQO1.
CONCLUSIONS: The above results together explain that five LC uterine perfusions can be used to establish a mouse model of clinical endometritis. CGA can treat clinical endometritis by activating Keap1/Nrf2 and inhibiting the NFκB signalling pathway.
METHODS: In this study, five LC uterine perfusions were selected to model clinical endometritis. The anti-inflammatory and antioxidant effects of CGA were clarified. Through HE staining, proinflammatory cytokines, blood testing, NFκB and Keap1/Nrf2 signalling pathways and other index changes to explore the protection mechanism of CGA.
KEY FINDINGS: After CGA treatment, the appearance, inflammatory damage and blood indicators of the mouse uterus returned to normal. Simultaneously, CGA could inhibit the activation of NFκB and reduce the release of inflammatory cytokines; CGA could also activate Keap1/Nrf2, promote the dissociation of Keap1 and Nrf2 and significantly increase the expression of the downstream genes HO-1 and NQO1.
CONCLUSIONS: The above results together explain that five LC uterine perfusions can be used to establish a mouse model of clinical endometritis. CGA can treat clinical endometritis by activating Keap1/Nrf2 and inhibiting the NFκB signalling pathway.