<scp>d</scp>-Mannose promotes recovery from experimental colitis by inducing AMPK phosphorylation to stimulate epithelial repair

Zhang, Haojie; Zhao, Xue; Gao, Yifei; Shi, Yao; Wei, Lina; Li, Jingxin; Liu, Chuanyong; Ma, Xuelian

doi:10.1039/d3fo03146b

Cited by 4 publications

(1 citation statement)

References 48 publications

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“…Endogenous OT might have a similar effect, as we found that the concentration of OT in plasma was significantly increased at 14 days following VCR treatment. We had previously reported that the elevated level of OT induced by D-mannose inhibited DSS-induced intestinal injury ( Shi et al, 2021 ; Zhang et al, 2024 ). Therefore, we speculated that VCR treatment promoted the local synthesis and secretion of OT in the intestine, which in return might have an endogenous protective effect on VCR-induced intestinal transit weakening.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of oxytocin on vincristine-induced gastrointestinal dysmotility in mice

Li,

Shi,

Zhu

et al. 2024

Front. Pharmacol.

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Aims: Vincristine (VCR), an antineoplastic drug, induces peripheral neuropathy characterized by nerve damage, limiting its use and reducing the quality of life of patients. VCR causes myenteric neuron damage, inhibits gastrointestinal motility, and results in constipation or paralytic ileus in patients. Oxytocin (OT) is an endogenous neuropeptide produced by the enteric nerve system, which regulates gastrointestinal motility and exerts neuroprotective effects. This study aimed to investigate whether OT can improve VCR-induced gastrointestinal dysmotility and evaluate the underlying mechanism.Methods: Mice were injected either with saline or VCR (0.1 mg/kg/d, i. p.) for 14 days, and OT (0.1 mg/kg/d, i.p.) was applied 1 h before each VCR injection. Gastrointestinal transit and the contractile activity of the isolated colonic segments were assessed. The concentration of OT in plasma was measured using ELISA. Immunofluorescence staining was performed to analyze myenteric neurons and reactive oxygen species (ROS) levels. Furthermore, the indicators of oxidative stress were detected. The protein expressions of Nrf2, ERK1/2, P-ERK1/2, p38, and P-p38 in the colon were tested using Western blot.Results: VCR reduced gastrointestinal transit and the responses of isolated colonic segments to electrical field stimulation and decreased the amount of neurons. Furthermore, VCR reduced neuronal nitric oxide synthase and choline acetyltransferase immunopositive neurons in the colonic myenteric nerve plexus. VCR increased the concentration of OT in plasma. Exogenous OT pretreatment ameliorated the inhibition of gastrointestinal motility and the injury of myenteric neurons caused by VCR. OT pretreatment also prevented the decrease of superoxide dismutase activity, glutathione content, total antioxidative capacity, and Nrf2 expression, the increase of ROS levels, and the phosphorylation of ERK1/2 and p38 MAPK following VCR treatment.Conclusion: Our results suggest that OT pretreatment can protect enteric neurons from VCR-induced injury by inhibiting oxidative stress and MAPK pathways (ERK1/2, p38). This may be the underlying mechanism by which it alleviates gastrointestinal dysmotility.

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Section: Discussionmentioning

confidence: 99%