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. 2024 Jul 17:11:1418899.
doi: 10.3389/fvets.2024.1418899. eCollection 2024.

Antioxidative effect of astragalosides on acute pancreatitis in mice

Xueting Hou  1 , Miao Yu  1 , Yang Xu  1 , Liuwei Wang  1 , Yishan Chen  1 , Ruisong Tao  1 , Qixin Zhang  1   2 , Yong Zhu  1   2
Affiliations

Antioxidative effect of astragalosides on acute pancreatitis in mice

Xueting Hou et al. Front Vet Sci. .

Abstract

Introduction: The research examined the antioxidative impact of astragalosides (AST) on experimental acute pancreatitis (AP) in mice. This study aims to assess the correlation between varying doses of astragalosides and superoxide dismutase (SOD) activity in an acute pancreatitis mouse model. By examining the interplay between astragaloside's protective effects and its antioxidant properties, we aim to deepen our understanding of its therapeutic potential in acute pancreatitis.

Methods: The AP model in mice was induced by retrograde injection of sodium deoxycholate into the biliary and pancreatic ducts. Serum amylase activity was monitored at various time points following induction. Furthermore, 24 hours post-induction, levels of serum nitric oxide (NO), superoxide dismutase (SOD) activity, and malondialdehyde (MDA) content in pancreatic tissue were assessed.

Results: The findings of this study illustrated that AST, while exhibiting a protective effect in experimental AP, could effectively lower the elevated serum NO levels, reduce MDA production, and enhance SOD activity in model mice. AST notably reduced MDA levels in the pancreatic tissue of AP mice, underscoring its ability to inhibit membrane peroxidation induced by oxygen free radicals. Furthermore, AST was observed to elevate SOD activity in scavenging oxygen free radicals in pancreatic tissue.

Conclusion: These findings suggest that AST enhances recovery in an experimental acute pancreatitis mouse model by exerting antioxidative effects.

Keywords: acute pancreatitis; antioxidative effect; astragalosides; mice; model.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Preparation of animal model of acute pancreatitis in mice.
Figure 2
Figure 2
Establishment of acute pancreatitis model. The standard control group showed no apparent pancreatic tissue injury after 24 h. In the AP model group, the pancreatic interstitium displayed saponification and necrosis. Pancreatic edema, saponification, and bleeding were markedly improved in the AST treatment group compared to the AP model group.
Figure 3
Figure 3
Serum amylase (AMS) levels at different time points in mice with acute pancreatitis (A) Serum amylase level at different time in Normal control group. (B) Serum amylase level at different time in AP model group. (C) Serum amylase level at different time in OCT positive control group. (D) Serum amylase level at different time in AST (20mg/kg). (E) Serum amylase level at different time in AST (40mg/kg). (F) Serum amylase level at different time in AST (20mg/kg).
Figure 4
Figure 4
Serum amylase (AMS) levels at different time points in mice with acute pancreatitis (A) Comparison of serum amylase levels in six groups before modeling. (B) Comparison of serum amylase levels among six groups at 6 hours. (C) Comparison of serum amylase levels among six groups at 12 h. (D) Comparison of serum amylase levels among six groups at 24 h.
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