Electroacupuncture at ST‐36 Protects Interstitial Cells of Cajal via Sustaining Heme Oxygenase‐1 Positive M2 Macrophages in the Stomach of Diabetic Mice

Tian, Lugao; Song, Shuangning; Zhu, Beibei; Liu, Shi

doi:10.1155/2018/3987134

Cited by 18 publications

(23 citation statements)

References 25 publications

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“…As we all know that ICC generates slow waves and leads to a contraction of smooth muscle, which is related to the GI motility the survival and functions of ICC strongly depend on the activation of receptor tyrosine kinase c‐Kit by mSCF . Our previous and current studies verified that EA can increase ICC numbers and maintaining the integrity of ICC network via mSCF/c‐Kit pathway in STZ‐induced diabetic mice . Interestingly, a few studies recently found that CNP/NPR‐B signaling was relevant to the mSCF/c‐Kit signal.…”

Section: Discussionsupporting

confidence: 70%

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Electroacupuncture promotes the gastrointestinal motility of diabetic mice by CNP/NPR‐B‐cGMP and PDE3A‐cGMP signaling

Song

et al. 2019

Neurogastroenterology Motil

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Background Electroacupuncture (EA) can promote gastrointestinal (GI) motility of diabetic mice, but the mechanism is not clearly elucidated. Natriuretic peptides (NPs) were related to the diabetes‐induced gut dysfunction of mice, which may be associated with ICC (interstitial cells of cajal). Besides, EA could increase the ICC of diabetic mice. Our aim was to explore whether EA can promote the gut motility by CNP/NPR‐B‐cGMP and PDE3A‐cGMP signaling in diabetic mice, and the relationship between NPs and ICC. Methods Wild C57BL/6 male mice were divided into five groups: control group, diabetic mellitus (DM group), diabetic mellitus plus sham EA group (SEA), diabetic mellitus plus low‐frequency EA group (LEA), and diabetic mellitus plus high‐frequency group (HEA). Gastrointestinal motility was assessed by gastric emptying and GI transit test. Immunofluorescence staining was applied to assess the expression level of CNP, NPR‐B, and c‐Kit. Western blot, PCR, and ELISA were used to detect the level of CNP, NPR‐B, PDE2A, PDE3A, c‐Kit, mSCF, and cGMP content. The correlativity between NPR‐B and mSCF was evaluated by Pearson's correlation and linear regression analyses. Key Results (a) EA could improve the GI dysfunction of diabetic mice. (b) CNP, NPR‐B, and cGMP contents were decreased, but the level of PDE3A, c‐Kit, and mSCF was increased in the EA groups. (c) There was a negative correlation between NPR‐B and mSCF among the groups. Conclusions and Inferences Electroacupuncture promotes the GI function by CNP/NPR‐B‐cGMP and PDE3A‐cGMP signaling in diabetic mice; up‐regulated mSCF/c‐Kit signaling by EA may be mediated partially via down‐regulation of CNP/NPR‐B signaling.

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Section: Discussionsupporting

confidence: 70%

“…26,27 Our previous and current studies verified that EA can increase ICC numbers and maintaining the integrity of ICC network via mSCF/c-Kit pathway in STZinduced diabetic mice. 28 Interestingly, a few studies recently found that CNP/NPR-B signaling was relevant to the mSCF/c-Kit signal.…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture promotes the gastrointestinal motility of diabetic mice by CNP/NPR‐B‐cGMP and PDE3A‐cGMP signaling

Song

et al. 2019

Neurogastroenterology Motil

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“…MDA has been taken as an indirect marker of oxidative stress [ 32 ]. In our experiments, MDA was significantly increased in diabetic rats, which was consistent with previously reported findings [ 15 ], and GEP could lower the level of MDA. SOD, a main antioxidant enzyme, plays a role in the destruction of free superoxide radicals and blocks free radical-induced damage [ 33 ].…”

Section: Discussionsupporting

confidence: 93%

“…In a rat model of streptozotocin-induced diabetes, impaired HO-1 induction in the gastric antrum induced disruption of the ICC network; thus, upregulated HO-1 expression could significantly restore the previously reduced ICC in the gastric antrum [ 14 ]. Although it is reported that EA could improve the expression of HO-1 in diabetic gastroparesis rats [ 15 ], the effects of GEP were to investigate as these two interventions had different mechanisms. We clarified that different pulse width with similar frequency GEP could promote the expression of the Nrf2/HO-1 signaling pathway, indicating the possible mechanism that GEP restore ICC in diabetic gastroparesis rats.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, in a study of diabetic gastroparesis model, it has been found that the downregulation of HO-1 could not resist oxidative stress injury, which leads to the destruction of ICCs network and delayed gastric emptying, but upregulation of HO-1 could repair the injury of ICCs and improve the delayed gastric emptying [ 13 , 14 ]. Similarly, Tian LG et al reported that the expression of HO-1 in gastric antrum of diabetic gastroparesis mice was significantly decreased, and EA could improve the expression of HO-1 and gastric motility [ 15 ]. Therefore, we speculate that GEP may play a key role in improving gastric motility disorder by upregulating HO-1 to repair ICC injury.…”

Section: Introductionmentioning

confidence: 99%

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Gastric Electrical Pacing Reduces Apoptosis of Interstitial Cells of Cajal via Antioxidative Stress Effect Attributing to Phenotypic Polarization of M2 Macrophages in Diabetic Rats

Wang

Zhao

Ying

et al. 2021

Oxidative Medicine and Cellular Longevity

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Background. Gastric electrical pacing (GEP) could restore interstitial cells of Cajal in diabetic rats. M2 macrophages contribute to the repair of interstitial cells of Cajal injury though secreting heme oxygenase-1 (HO-1). The aim of the study is to investigate the effects and mechanisms of gastric electrical pacing on M2 macrophages in diabetic models. Methods. Sixty male Sprague-Dawley rats were randomized into control, diabetic (DM), diabetic with the sham GEP (DM+SGEP), diabetic with GEP1 (5.5 cpm, 100 ms, 4 mA) (DM+GEP1), diabetic with GEP2 (5.5 cpm, 300 ms, 4 mA) (DM+GEP2), and diabetic with GEP3 (5.5 cpm, 550 ms, 4 mA) (DM+GEP3) groups. The apoptosis of interstitial cells of Cajal and the expression of macrophages were detected by immunofluorescence technique. The expression levels of the Nrf2/HO-1 and NF-κB pathway were evaluated using western blot analysis or immunohistochemical method. Malonaldehyde, superoxide dismutase, and reactive oxygen species were tested to reflect the level of oxidative stress. Results. Apoptosis of interstitial cells of Cajal was increased in the DM group but significantly decreased in the DM+GEP groups. The total number of macrophages was almost the same in each group. In the DM group, M1 macrophages were increased and M2 macrophages were decreased. However, M2 macrophages were dramatically increased and M1 macrophages were reduced in the DM+GEP groups. Gastric electrical pacing improved the Nrf2/HO-1 pathway and downregulated the phosphorylation of NF-κB. In the DM group, the levels of malonaldehyde and reactive oxygen species were elevated and superoxide dismutase was lowered, while gastric electrical pacing reduced the levels of malonaldehyde and reactive oxygen species and improved superoxide dismutase. Conclusion. Gastric electrical pacing reduces apoptosis of interstitial cells of Cajal though promoting M2 macrophages polarization to play an antioxidative stress effect in diabetic rats, which associates with the activated Nrf2/HO-1 pathway and the phosphorylation of NF-κB pathway.

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New insights into muscularis macrophages in the gut: from their origin to therapeutic targeting

et al. 2023

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Electroacupuncture at ST‐36 Protects Interstitial Cells of Cajal via Sustaining Heme Oxygenase‐1 Positive M2 Macrophages in the Stomach of Diabetic Mice

Cited by 18 publications

References 25 publications

Electroacupuncture promotes the gastrointestinal motility of diabetic mice by CNP/NPR‐B‐cGMP and PDE3A‐cGMP signaling

Electroacupuncture promotes the gastrointestinal motility of diabetic mice by CNP/NPR‐B‐cGMP and PDE3A‐cGMP signaling

Gastric Electrical Pacing Reduces Apoptosis of Interstitial Cells of Cajal via Antioxidative Stress Effect Attributing to Phenotypic Polarization of M2 Macrophages in Diabetic Rats

New insights into muscularis macrophages in the gut: from their origin to therapeutic targeting

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