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Copyright (c) 2023 Ye Zeng
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Anisodamine hydrobromide attenuates oxidative stress and proinflammatory cytokines in septic rats induced by cecal ligation and puncture
Corresponding Author(s) : Ye Zeng
Cellular and Molecular Biology,
Vol. 68 No. 12: Issue 12
Abstract
We previously demonstrated that anisodamine hydrobromide (Ani HBr) ameliorates septic organ injury induced by lipopolysaccharide. The present study is aimed to explore the role of Ani HBr in protecting the organs against inflammation and oxidative stress in septic rats induced by cecal ligation and puncture. A total of forty-two rats were randomly divided into sham (sham operation), septic shock, Ani HBr, atropine, and racemic anisodamine (Rac Ani) groups. Ani HBr (1.8, 3.6, and 5.4 mg/kg), atropine (5.4 mg/kg), and Rac Ani (5.4 mg/kg) were administrated to septic rats. After 24 h, the plasma and organs including brain, heart, liver, lung, kidney, and intestine were obtained. Then, the H&E staining and TUNEL staining were performed. The proinflammatory factors TNF-α and IL-6 and oxidative stress markers superoxide dismutase (SOD) and malondialdehyde (MDA)in plasma were detected by ELISA. H&E staining showed that the tissues in the brain, heart, liver, lung, kidney, and intestine in the septic shock group were seriously damaged. Consistently, TUNEL staining showed an increase of apoptotic cells in those tissues. Ani HBr treatment alleviated the injury and apoptotic cells in all those organs in septic rats. Ani HBr, atropine, and Rac Ani reduced the plasma TNF-α and IL-6 levels in septic rats, whereas 5.4 mg/kg Ani HBr reduced the cytokines more than Rac Ani. Ani HBr raised SOD activity and reduced plasma MDA levels in a concentration-dependent manner, which at 5.4 mg/kg were greater than atropine and Rac Ani. Therefore, anisodamine hydrobromide suppressed the proinflammatory cytokines and oxidative stress, thereby alleviating organ injury in rats with septic shock. Moreover, the therapeutic effect of Ani HBr is more powerful than that of atropine or Rac Ani, which suggests that Ani HBr is a preferred treatment for septic shock.
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