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经导管肉毒杆菌毒素注射抑制实验性急性胰腺炎的炎症。

Intraductal botulinum toxin injection suppressed the inflammation in experimental acute pancreatitis.

机构信息

Department of Organ Transplantation, Acıbadem Mehmet Ali Aydınlar University, Atakent Hospital, İstanbul-Türkiye.

Department of Biochemistry, Kocaeli University Faculty of Medicine, Kocaeli-Türkiye.

出版信息

Ulus Travma Acil Cerrahi Derg. 2022 Dec;28(12):1659-1666. doi: 10.14744/tjtes.2021.90140.

DOI:10.14744/tjtes.2021.90140
PMID:36453789
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10198305/
Abstract

BACKGROUND

Acute pancreatitis (AP) is inflammation of pancreas in which pancreas enzymatic activity is increased. Parasym-pathetic innervation of pancreas plays an important role in several functions of pancreas. Botulinum toxin (BTx) might be a tool to suppress the pancreas activity in AP.

METHODS

In the preliminary experimental study, BTx (15U/kg) was administered directly and intraductal ways. After 10 days, blood amylase, lipase, trypsinogen, insulin, and glucagon levels were compared and no significant difference was seen between groups. Intraductal BTx administration is preferred for experimental AP model in rats; control, AP, intraductal BTx, and AP with Intraductal BTx (AP+BTx). AP was created by intraperitoneal injection of cerulean 20 µg/kg/injection (5 times). After 24 h, serum amylase, lipase, IL-6, IL-1β, TNF-α, and IL-10 were measured and pancreas tissue was evaluated for inflammation and necrosis.

RESULTS

Mean serum amylase, lipase IL-6, IL-1β, and TNF-α levels of the AP group were significantly higher compared to the other groups (p<0.05). However, there was no significant difference between the amylase and lipase levels of control, BTx, and AP+BTx groups. Serum insulin and glucagon levels in AP group were significantly higher than control and BTx groups (p<0.05). However, there is no significant difference between the insulin and glucagon levels of AP and AP+BTx groups. in pathological evaluation. In AP+ BTx group, there is less amount of centrilobular necrosis and there is mild inflammation and hyperplasia of pancreatic duct epithelium.

CONCLUSION

Administration of intraductal BTx suppressed the AP without making significant suppression in endogenous activity of pancreas.

摘要

背景

急性胰腺炎(AP)是胰腺炎症,其中胰腺酶活性增加。胰腺的副交感神经支配在胰腺的几种功能中起着重要作用。肉毒杆菌毒素(BTx)可能是抑制 AP 中胰腺活性的工具。

方法

在初步的实验研究中,BTx(15U/kg)直接和经导管给药。10 天后,比较各组的血淀粉酶、脂肪酶、胰蛋白酶原、胰岛素和胰高血糖素水平,未见组间差异。经导管 BTx 给药是大鼠实验性 AP 模型的首选方法;对照组、AP 组、经导管 BTx 组和 AP 联合经导管 BTx 组(AP+BTx)。通过腹腔注射蓝斑 20µg/kg/次(5 次)建立 AP。24 小时后,测量血清淀粉酶、脂肪酶、IL-6、IL-1β、TNF-α和 IL-10,评估胰腺组织的炎症和坏死程度。

结果

与其他组相比,AP 组的血清淀粉酶、脂肪酶、IL-6、IL-1β和 TNF-α水平均显著升高(p<0.05)。然而,对照组、BTx 组和 AP+BTx 组的淀粉酶和脂肪酶水平无显著差异。AP 组的血清胰岛素和胰高血糖素水平明显高于对照组和 BTx 组(p<0.05)。然而,AP 组和 AP+BTx 组的胰岛素和胰高血糖素水平无显著差异。在组织病理学评估中,在 AP+BTx 组中,中心小叶坏死程度较轻,且胰腺导管上皮有轻度炎症和增生。

结论

经导管 BTx 给药可抑制 AP,而不会对胰腺内源性活性产生显著抑制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee7/10198305/dad7251a0f9a/TJTES-28-1659-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee7/10198305/4807c2129953/TJTES-28-1659-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee7/10198305/b393e3b8dc5b/TJTES-28-1659-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee7/10198305/3fe09249d296/TJTES-28-1659-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee7/10198305/38764a494f9d/TJTES-28-1659-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee7/10198305/f682a6b005f6/TJTES-28-1659-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee7/10198305/4a6c47c00404/TJTES-28-1659-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee7/10198305/dad7251a0f9a/TJTES-28-1659-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee7/10198305/4807c2129953/TJTES-28-1659-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee7/10198305/b393e3b8dc5b/TJTES-28-1659-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee7/10198305/3fe09249d296/TJTES-28-1659-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee7/10198305/38764a494f9d/TJTES-28-1659-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee7/10198305/f682a6b005f6/TJTES-28-1659-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee7/10198305/4a6c47c00404/TJTES-28-1659-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ee7/10198305/dad7251a0f9a/TJTES-28-1659-g007.jpg

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