Validation experiment designed to validate causal mechanisms targeting CHAT, CHRNA7 in mice. Primary outcome: colitis severity reduction measured by body weight loss and colon tissue damage
This study investigated the therapeutic effects of electroacupuncture (EA) at the Shangjuxu (ST37) acupoint on experimentally induced colitis in mice and examined the underlying mechanisms involving the vagal cholinergic anti-inflammatory pathway. Mice were divided into four groups: control, model (DSS-induced colitis), EA treatment, and MLA group (EA treatment with α7nAChR antagonist). Colitis was induced by providing mice with 2.5% dextran sodium sulfate (DSS) solution for 7 days. The researchers assessed colitis severity through multiple parameters including body weight changes, colon length measurements, and histopathological examination using H&E staining. Cytokine levels in proximal colon tissue were quantified using MSD assay. The study employed immunofluorescence techniques to evaluate the activation of ChAT-positive neurons in the dorsal motor nucleus of the vagus (DMV) and examined cholinergic markers in the colon. Anatomical relationships between ChAT-positive fibers and α7nAChR-positive cells were investigated. Additionally, electrophysiological recordings were performed to measure vagal efferent fiber activity.
...Mice received 2.5% DSS solution for 7 days to induce colitis, followed by electroacupuncture treatment at ST37 acupoint. Assessment included body weight monitoring, colon length measurement, H&E staining, cytokine analysis by MSD assay, immunofluorescence for ChAT and α7nAChR markers, and electrophysiological recording of vagal activity.
EA treatment was expected to and did reduce colitis severity, decrease pro-inflammatory cytokines, activate ChAT-positive neurons in DMV, restore α7nAChR levels, and increase vagal efferent activity through cholinergic anti-inflammatory mechanisms
Significant reduction in body weight loss, decreased colon tissue damage, reduced pro-inflammatory cytokine levels, increased ChAT neuron activation, and restored α7nAChR expression
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