Kupffer cells play a crucial role in monocrotaline-induced liver injury by producing TNF-α

Cao, Yuhan; Li, Meng; Wu, Shouyan; Xu, Junjiu; Wang, Wenjie; Qi, Xinming; Ren, Jin; Sun, Jianhua; Chen, Jing; Gong, Likun

doi:10.1016/j.tox.2022.153101

Cited by 2 publications

(1 citation statement)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The observed increase in liver weight after monocrotaline administration may be related to the structural remodeling of this organ. Monocrotaline can induce liver injury directly via the destruction of liver sinusoidal endothelial cells [ 20 , 21 , 22 ] or indirectly due to the development of the right ventricular hypertrophy and consequent liver congestion [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

Monocrotaline-Induced Pulmonary Arterial Hypertension and Bosentan Treatment in Rats: Focus on Plasma and Erythrocyte Parameters

et al. 2022

View full text Add to dashboard Cite

The objective of our study was to contribute to the characterization of monocrotaline-induced pulmonary arterial hypertension (PAH) in a rat model, with emphasis on the renin–angiotensin–aldosterone system, parameters of oxidative stress, the activity of matrix metalloproteinases, and erythrocyte parameters. Moreover, we aimed to analyze the effects of bosentan. Experiments were performed on 12-week-old male Wistar rats randomly assigned to 3 groups: control, monocrotaline-treated (60 mg/kg), and monocrotaline combined with bosentan (300 mg/kg/day). Our study confirmed the well-known effects of monocrotaline administration on lungs and the right ventricle, as well as pulmonary arterial pressure. In addition, we observed activation of the alternative pathway of the renin–angiotensin system, namely an increase in angiotensin (Ang) 1–7 and Ang 1-5 together with an increase in Ang I, but without any change in Ang II level, and downregulation of aldosterone 4 weeks after monocrotaline administration. For the first time, modifications of erythrocyte Na,K-ATPase enzyme kinetics were demonstrated as well. Our observations do not support data obtained in PAH patients showing an increase in Ang II levels, increase in oxidative stress, and deterioration in RBC deformability. Although bosentan primarily targets the vascular smooth muscle, our study confirmed its antioxidant effect. The obtained data suggest that besides the known action of bosentan, it decreases heart rate and increases erythrocyte deformability, and hence could have a beneficial hemodynamic effect in the PAH condition.

show abstract