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清胰汤防治重症急性胰腺炎心肌损伤。

Qingyi decoction protects against myocardial injuries induced by severe acute pancreatitis.

机构信息

Department of Vascular Surgery, The Second Affiliated Hospital of Dalian Medical University, Dalian 116027, Liaoning Province, China.

Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba 3058575, Japan.

出版信息

World J Gastroenterol. 2020 Mar 28;26(12):1317-1328. doi: 10.3748/wjg.v26.i12.1317.

DOI:10.3748/wjg.v26.i12.1317
PMID:32256019
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7109276/
Abstract

BACKGROUND

We studied the protective effects of Qingyi decoction (QYD) (a Traditional Chinese Medicine) against severe acute pancreatitis (SAP)-induced myocardial infarction (MI).

AIM

To study the function and mechanism of QYD in the treatment of myocardial injuries induced by SAP.

METHODS

Ultrasonic cardiography, hematoxylin and eosin staining, immunohistochemistry, qRT-PCR, western blot, enzyme-linked immunosorbent assays, and apoptosis staining techniques were used to determine the effects of QYD following SAP-induced MI in Sprague-Dawley rats.

RESULTS

Our SAP model showed severe myocardial histological abnormalities and marked differences in the symptoms, mortality rate, and ultrasonic cardiography outputs among the different groups compared to the control. The expression of serum cytokines [interleukin (IL)-1ß, IL-6, IL-8, IL-12, amyloid β, and tumor necrosis factor-α] were significantly higher in the SAP versus QYD treated group ( 0.05 for all). STIM1 and Orai1 expression in myocardial tissue extracts were significantly decreased post QYD gavage ( < 0.001). There was no significant histological difference between the 2-aminoethyl diphenylborinate inhibitor and QYD groups. The SAP group had a significantly higher apoptosis index score compared to the QYD group ( < 0.001).

CONCLUSION

QYD conferred cardio-protection against SAP-induced MI by regulating myocardial-associated protein expression (STIM1 and Orai1).

摘要

背景

我们研究了清胰汤(QYD)(一种中药)对重症急性胰腺炎(SAP)诱导性心肌梗死(MI)的保护作用。

目的

研究 QYD 治疗 SAP 引起的心肌损伤的功能和机制。

方法

采用超声心动图、苏木精-伊红染色、免疫组织化学、qRT-PCR、western blot、酶联免疫吸附试验和凋亡染色技术,确定 QYD 对 SAP 诱导的 MI 后 Sprague-Dawley 大鼠的影响。

结果

我们的 SAP 模型显示严重的心肌组织学异常,与对照组相比,各组之间的症状、死亡率和超声心动图结果差异显著。与 QYD 处理组相比,SAP 组血清细胞因子[白细胞介素(IL)-1β、IL-6、IL-8、IL-12、淀粉样β和肿瘤坏死因子-α]的表达显著升高(均为 0.05)。心肌组织提取物中 STIM1 和 Orai1 的表达明显降低(均<0.001)。2-氨基乙基二苯硼酸盐抑制剂组和 QYD 组之间无明显的组织学差异。SAP 组的凋亡指数评分明显高于 QYD 组(均<0.001)。

结论

QYD 通过调节心肌相关蛋白表达(STIM1 和 Orai1)对 SAP 诱导的 MI 提供心脏保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/052d/7109276/a3ab611554ae/WJG-26-1317-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/052d/7109276/e64954ce005f/WJG-26-1317-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/052d/7109276/a3ab611554ae/WJG-26-1317-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/052d/7109276/e64954ce005f/WJG-26-1317-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/052d/7109276/a3ab611554ae/WJG-26-1317-g004.jpg

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