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. 2021 Jun;21(6):548.
doi: 10.3892/etm.2021.9980. Epub 2021 Mar 24.

Curcumin relieves mice gastric emptying dysfunction induced by L-arginine and atropine through interstitial cells of Cajal

Peng Lin  1 , Baitao Li  2 , Junli Ye  1 , Fangfang Shang  3 , Hui Zhao  3 , Jing Xie  4 , Xiaoling Yu  1
Affiliations

Curcumin relieves mice gastric emptying dysfunction induced by L-arginine and atropine through interstitial cells of Cajal

Peng Lin et al. Exp Ther Med. 2021 Jun.

Abstract

Curcumin is natural polyphenol from Curcuma longa rhizomes with several biological properties. Our previous studies demonstrated that curcumin inhibited functional gastric emptying disorders induced by L-arginine, the precursor of nitric oxide (NO), and atropine, an acetylcholine receptor (AChR) blocker. However, the mechanism of action of curcumin remains unclear. In the present study, mouse models of functional gastric emptying disorders induced by L-arginine and atropine were used to examine changes in interstitial cells of Cajal (ICC) and NO- and ACh-mediated regulation of gastrointestinal motility. Curcumin pre-treatment ameliorated the gastric emptying rate in mice treated with L-arginine or atropine (P<0.01). NO content and NO synthase activity significantly increased in the stomachs of L-arginine-treated mice, compared with controls (P<0.01). Acetylcholinesterase activity (P<0.01) and mRNA expression (P<0.01), as well as AChR mRNA levels (P<0.05) significantly decreased following atropine treatment. Moreover, in both models, the levels of c-kit, anoctamin 1 and connexin 43 significantly decreased in the stomach (P<0.01). Conversely, curcumin pre-treatment inhibited the changes induced by L-arginine and atropine (P<0.01 or P<0.05). By affecting the production of exogenous NO, the effects of Ach-AchR and the biomarkers of ICC, curcumin relieves the gastric emptying dysfunction in mice.

Keywords: acetylcholine; atropine; curcumin; functional gastrointestinal disorders; nitric oxide.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Figure 1
Figure 1
Changes in gastric emptying rates and the relative biomarkers of NO following Cur and L-arg treatment. (A) Changes in gastric emptying rates. (B) NO content. (C) TNOS and (C) iNOS activity. Data are presented as the mean ± SD; ##P<0.01 vs. Control; **P<0.01 vs. L-arg. Cur, curcumin; gprot, grams of protein; iNOS, inducible NO synthase; L-arg, L-arginine; mgprot, milligrams of protein; NO, nitric oxide; TNOS, total NO synthase.
Figure 2
Figure 2
Changes in relative expression levels interstitial cells of Cajal markers following Cur and L-arg treatment. (A) Reverse transcription-quantitative PCR and (B) Western blot analysis. Data are presented as the mean ± SD; #P<0.05 and ##P<0.01, vs. Control; *P<0.05 and **P<0.01 vs. L-arg. Ano1, anoctamin 1; CX43, connexin 43; Cur, curcumin; L-arg, L-arginine.
Figure 3
Figure 3
Changes in gastric emptying rates and the relative biomarkers of ACh following Cur and Atr treatment. (A) Changes in gastric emptying rates. (B) Activity levels of AChE. (C) AChE and AChR mRNA expression levels. Data are presented as the mean ± SD; #P<0.05 and ##P<0.01 vs. Control; *P<0.05 and **P<0.01 vs. Atr. AChE, acetylcholinesterase; AChR, acetylcholine receptor; Atr, atropine; Cur, curcumin; mgprot, milligrams of protein.
Figure 4
Figure 4
Changes in relative expression levels of interstitial cells of Cajal markers following Cur and Atr treatment. (A) Reverse transcription-quantitative PCR and (B) Western blot analysis. Data are presented as the mean ± SD; #P<0.05 and ##P<0.01, vs. Control; *P<0.05 and **P<0.01 vs. Atr. Ano1, anoctamin 1; atr, atropine; Cur, curcumin; CX43, connexin 43.
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