4.6 Article

Electroacupuncture Ameliorates Acute Pancreatitis: A Role for the Vagus Nerve-Mediated Cholinergic Anti-Inflammatory Pathway

期刊

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fmolb.2021.647647

关键词

electroacupuncture; pancreatitis; vagus nerve; α 7 nicotinic acetylcholine receptor; anti-inflammation

资金

  1. National Natural Science Foundation of China [81704164]
  2. Yong Natural Science Program of Nanjing University of ChineseMedicine [NZY81704164]

向作者/读者索取更多资源

The study found that electroacupuncture can increase vagus nerve activity, suppress systemic inflammation, alleviate pancreatic histopathological manifestations, and increase the frequency of alpha 7nAchR. However, vagotomy or treatment with an alpha 7nAChR antagonist can weaken the therapeutic effects of electroacupuncture.
Organ failure resulting from excessive inflammation is the leading cause of death in the early phase of acute pancreatitis (AP). The autonomic nervous system was reported to be involved in AP, and the vagus nerve could exert anti-inflammatory effects through alpha 7 nicotinic acetylcholine receptor (alpha 7nAChR) signaling. Acupuncture has been widely used in traditional Asian medicine, and recent studies suggested the inflammation modulating effect of electroacupuncture (EA) might be mediated by the autonomic nervous system. In this study, we aimed to investigate the effects of EA in AP animal models. Two independent AP mouse models were used, namely, caerulein hyperstimulation and pancreatic duct ligation. We found that EA at Zusanli acupoint increased vagus nerve activity, suppressed systemic inflammation, and alleviated the histopathological manifestations and leukocyte infiltrations of the pancreas. Induction of AP resulted in a remarkable decrease in the frequency of alpha 7nAchR(+) macrophages in the pancreas, while EA counteracted this phenomenon. The anti-inflammatory, pancreatic protective and upregulation of alpha 7nAchR effects of EA were reduced in mice with vagotomy. Moreover, the therapeutic effects of EA were attenuated in mice treated with methyllycaconitine citrate, a selective alpha 7nAChR antagonist. Taken together, EA could modulate inflammation, thereby exerting protective effects in AP. The mechanism may include activating the vagus nerve through the cholinergic anti-inflammatory pathway.

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