1.Effects and mechanisms of the aqueous extract of Artemisia capillaris(Yin Chen)in alleviating liver injury induced by LPS combined with D-GalN in mice
Yanan CHUO ; Jiaxue SHEN ; Weiyu YAO ; Xiao WANG ; Yongzhan BAO ; Jinxu TANG ; Wanyu SHI
Chinese Journal of Veterinary Science 2025;45(10):2239-2245,2263
In order to investigate the mitigating effect of Yin Chen aqueous extract on liver injury induced by LPS combined with D-GalN in mice,a mouse liver injury model was established by in-traperitoneal injection of LPS and D-GalN,and the mice were group-fed by instillation of saline,bi-phenyl dibenzyl ester,and Yin Chen aqueous extract with different concentrations of LPS and D-GalN.The liver index of mice was calculated,pathological tissue sections were observed,and the expression of ALT,AST,inflammatory cytokines,oxidative stress,hepatic enzymes,and IL-17/TNF pathway were detected in serum to investigate the effects and mechanisms of the aqueous ex-tracts of Yin Chen in alleviating the liver injury in mice.The results showed that the liver index of mice in the model group was significantly elevated,the serum levels of ALT and AST were signifi-cantly elevated,the levels of IL-iβ,IL-8 and TNF-α in liver tissue were significantly elevated,the levels of IL-4 were significantly reduced,the levels of GSH-Px,CAT and SOD were significantly reduced,the levels of ROS and MDA were significantly elevated,CYP2E1 and CYP1A2 protein content and mRNA expression were significantly up-regulated,and the expression levels of TNF,TNFR1,IL-17A,ACT1 and IL-6 mRNA were significantly up-regulated.The study showed that the aqueous extract of Yin Chen had a certain alleviating effect on the liver injury caused by LPS combined with D-GalN in mice.The mechanism of action includes decreasing the metabolic level of hepatic drug enzymes,alleviating oxidative stress,inhibiting the expression of IL-17/TNF pathway and down-regulating the level of inflammatory factors in mice.
2.Prenatal BPA exposure in maternal rabbits impairs reproductive function in F1 fe-male offspring through oxidative stress and inflammatory responses
Qianhui ZHAO ; Jialu PAN ; Yanan CHUO ; Chenggong LIU ; Xiao WANG ; Wanyu SHI ; Yongzhan BAO
Chinese Journal of Veterinary Science 2025;45(6):1314-1321
Bisphenol A(BPA)is an environmental endocrine disruptor commonly found in industri-al products such as plastics,resin coatings,and paper coatings,and it poses potential reproductive hazards.Despite extensive research,studies examining its effects on the F1 generation of rabbits are limited.This study established a BPA exposure model in pregnant female rabbits to investigate its impact on reproductive hormones,apoptosis,oxidative stress,inflammatory responses,and tissue integrity in weaned female offspring.The results indicate that BPA exposure induces oxidative stress and inflammation in F1 rabbits,disrupts hormonal balance,and affects antioxidant enzymes and inflammatory mediators through the modulation of the Nrf2 and NF-κB signaling pathways,ultimately leading to apoptosis and tissue damage.
3.Prenatal BPA exposure in maternal rabbits impairs reproductive function in F1 fe-male offspring through oxidative stress and inflammatory responses
Qianhui ZHAO ; Jialu PAN ; Yanan CHUO ; Chenggong LIU ; Xiao WANG ; Wanyu SHI ; Yongzhan BAO
Chinese Journal of Veterinary Science 2025;45(6):1314-1321
Bisphenol A(BPA)is an environmental endocrine disruptor commonly found in industri-al products such as plastics,resin coatings,and paper coatings,and it poses potential reproductive hazards.Despite extensive research,studies examining its effects on the F1 generation of rabbits are limited.This study established a BPA exposure model in pregnant female rabbits to investigate its impact on reproductive hormones,apoptosis,oxidative stress,inflammatory responses,and tissue integrity in weaned female offspring.The results indicate that BPA exposure induces oxidative stress and inflammation in F1 rabbits,disrupts hormonal balance,and affects antioxidant enzymes and inflammatory mediators through the modulation of the Nrf2 and NF-κB signaling pathways,ultimately leading to apoptosis and tissue damage.
4.Effects and mechanisms of the aqueous extract of Artemisia capillaris(Yin Chen)in alleviating liver injury induced by LPS combined with D-GalN in mice
Yanan CHUO ; Jiaxue SHEN ; Weiyu YAO ; Xiao WANG ; Yongzhan BAO ; Jinxu TANG ; Wanyu SHI
Chinese Journal of Veterinary Science 2025;45(10):2239-2245,2263
In order to investigate the mitigating effect of Yin Chen aqueous extract on liver injury induced by LPS combined with D-GalN in mice,a mouse liver injury model was established by in-traperitoneal injection of LPS and D-GalN,and the mice were group-fed by instillation of saline,bi-phenyl dibenzyl ester,and Yin Chen aqueous extract with different concentrations of LPS and D-GalN.The liver index of mice was calculated,pathological tissue sections were observed,and the expression of ALT,AST,inflammatory cytokines,oxidative stress,hepatic enzymes,and IL-17/TNF pathway were detected in serum to investigate the effects and mechanisms of the aqueous ex-tracts of Yin Chen in alleviating the liver injury in mice.The results showed that the liver index of mice in the model group was significantly elevated,the serum levels of ALT and AST were signifi-cantly elevated,the levels of IL-iβ,IL-8 and TNF-α in liver tissue were significantly elevated,the levels of IL-4 were significantly reduced,the levels of GSH-Px,CAT and SOD were significantly reduced,the levels of ROS and MDA were significantly elevated,CYP2E1 and CYP1A2 protein content and mRNA expression were significantly up-regulated,and the expression levels of TNF,TNFR1,IL-17A,ACT1 and IL-6 mRNA were significantly up-regulated.The study showed that the aqueous extract of Yin Chen had a certain alleviating effect on the liver injury caused by LPS combined with D-GalN in mice.The mechanism of action includes decreasing the metabolic level of hepatic drug enzymes,alleviating oxidative stress,inhibiting the expression of IL-17/TNF pathway and down-regulating the level of inflammatory factors in mice.

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