相关实验视频
Updated: Sep 10, 2025

Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice
Published on: June 28, 2021
通过驱动病态胰腺分泌而加剧急性胰腺炎
Jie Ye1, Yiting Huang1, Xueqiang Liu1
1School of Medicine & Health Sciences, Guangzhou Huashang College, Guangzhou, 511300, People's Republic of China.
在小鼠中,Schisandrin B (SchB) 意外地使严重的急性胰腺炎 (SAP) 恶化. 这种天然化合物增加了消化酶的产生,导致胰腺损伤和自消化.
科学领域:
- 药理学
- 胃肠病学
- 分子生物学
背景情况:
- 希桑德林B (SchB) 是一种具有被证实的器官保护性质的天然质.
- 它在严重急性胰腺炎 (SAP) 中的潜在治疗作用尚未被研究.
研究的目的:
- 在严重急性胰腺炎 (SAP) 的小鼠模型上研究Schisandrin B (SchB) 的作用.
主要方法:
- 使用了由caerulein诱导的小鼠模型.
- 小鼠接受了施山德林B (30和60毫克/公斤) 的治疗.
- 分析包括组织学,生物化学和转录学 (RNA-seq) 评估.
主要成果:
- 斯基桑德林B显著加剧了胰腺炎,增加了胀,亡和炎症.
- 在接受SchB治疗的小鼠中,血清α-氨基酶水平显著升高.
- RNA-seq显示胰腺分泌途径基因的上调,包括消化酶,以及流基因Atp2a3的下调.
结论:
- 与预期的保护作用相反,西桑德林B会加剧急性胰腺炎.
- 该机制涉及转录上调消化酶的产生,可能导致细胞内过载和增强自消化.
- 在胰腺疾病中应谨慎使用SchB,因为它具有特定环境的有害作用.
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