Fig 1.
Schematic representation delineating the experimental design, key interventions, and analytical approaches employed in the investigation of acute gastric mucosal injury in rats.
Fig 2.
Analytical workflow for Evans blue dye extravasation in rat models of AGMI.
Fig 2 presents a detailed workflow for assessing EB dye extravasation in rat models of AGMI. This comprehensive process encompasses the extraction, quantification, and spatial analysis of EB dye from the cutaneous layers of AGMI-affected rats. A. The establishment of a geospatial coordinate grid facilitates the systematic mapping of EB extravasation across the skin. Notably, rats presenting with scraping injuries were rigorously excluded from the analysis to preclude confounding effects and ensure the reliability of data related to disease-specific EB extravasation. B. A schematic overview of the methodological steps adopted for the analysis. C. A depiction of the factor analysis approach, exemplified by the group treated with 0.50 M HCl to induce AGMI. D. A diagrammatic representation of the cutaneous regions demarcated for EB dye accumulation assessment.
Fig 3.
Gastric tissue damage in rats following gavage with hydrochloric acid: Effects of concentration and modeling time.
Fig 3 captures the alterations in gastric tissue morphology resulting from gavage administration of hydrochloric acid (HCl) in rats, with the extent of damage modulated by both the concentration of HCl and the duration of the modeling procedure. Histopathological insights are provided through hematoxylin and eosin (H&E) staining (n = 6 per group). A. A schematic representation of the rat modeling protocol employed to induce gastric mucosal injury. B. Histopathological micrographs at 100 × magnification, demonstrating the concentration-specific tissue damage in the stomach, as evidenced by H&E staining, and ulcer index. C. A diagram highlighting the temporal impact of HCl exposure on gastric mucosa morphology. D. Histopathological micrographs at 100 × magnification, showcasing the time-dependent evolution of gastric tissue damage following HCl gavage, as delineated by H&E staining, and ulcer index.
Fig 4.
Cluster analysis of cutaneous Evans blue extravasation points in rats with AGMI.
Fig 4 illustrates the cluster analysis of Evans Blue (EB) dye extravasation points on the body surface of rats with induced gastric mucosal injury, depicting the patterns of vascular leakage in relation to hydrochloric acid (HCl) concentration and exposure time (n = 6 per group). A. A schematic representation of the rat modeling protocol employed to induce gastric mucosal injury. B. A visual summary of the cluster analysis results, highlighting the patterns of EB dye extravasation across the rats’ body surface. C. Correlation analysis between the clustering of EB extravasation points and the variables of HCl concentration and duration of exposure.
Fig 5.
Factor analysis of temporal effects on gastric mucosal injury in rats.
Fig 5 showcases a segment of the comprehensive factor analysis undertaken to decode the temporal influence on the severity of gastric mucosal injury in rat models (n = 6 per group).
Fig 6.
Repeated measures variance analysis of feature regions 11 and 11’.
Fig 6 delineates the outcomes of a repeated measures analysis of variance (ANOVA) performed on Feature Regions 11 (FR-11) and 11’ (FR-11’).
Fig 7.
Mapping neuroinflammatory responses on rat dorsal surfaces post-AGMI.
Fig 7 synthesizes the investigation of neuroinflammatory mediator expression across a range of dorsal cutaneous regions in rats subjected to AGMI. A. Schematic representation of the methodological approach employed to investigate neuroinflammatory responses. B. Schematic localization of the multiple dorsal body surface areas assessed for neuroinflammatory activity in the rat model. C. Histological images of gastric tissue from both AGMI-induced and control rats, stained with Hematoxylin and Eosin (H&E) at 100x magnification. D. Comparative evaluation of nociceptive neuropeptides and sensitizers in predefined cutaneous regions between control groups and AGMI-treated rats (n = 6 per group). E. Immunofluorescent localization of 5-HT and CGRP in the cutaneous FR of rats with AGMI (n = 3 per group).
Fig 8.
Influence of Electroacupuncture at Feature Regions on Gastric Mucosal Healing in AGMI Rats.
Fig 8 examines the therapeutic efficacy of electroacupuncture (EA) applied at feature regions (FR) on healing gastric mucosal lesions in a rat model of AGMI (n = 6 per group). A. A schematic representation of the rat modeling protocol employed to induce gastric mucosal injury. B. A diagram indicating the exact locations of EA intervention on the rats’ body. C. Histological sections of the gastric mucosa after a seven-day course of EA treatment, stained with Hematoxylin and Eosin (H&E) and presented at 100x magnification. D. A comparative evaluation of cytokine concentrations in both serum and gastric tissue samples.
Fig 9.
Potential mechanistic pathways of neurogenic skin responses post-visceral sensitization following AGMI.
Fig 9 outlines a conceptual framework illustrating the mechanistic pathways involved in the development of neurogenic skin responses following visceral sensitization subsequent to AGMI. In pathological conditions, abnormal excitatory signals originating from the viscera are transmitted via dorsal root neurons, subsequently activating spinal dorsal horn cells and propagating to peripheral nerve terminals. Upon entering the spinal dorsal horn, these nerve impulses activate additional dorsal root ganglion cells through interneurons and are then transmitted to peripheral nerves via dorsal root reflexes. Furthermore, abnormal excitatory signals from diseased viscera are conveyed to peripheral nerves through somatovisceral reflexes via dorsal root branches. Upon reaching the periphery, these impulses stimulate nerve terminals to release inflammatory mediators such as SP and CGRP, thereby eliciting a neurogenic inflammatory response. Subsequently, SP further induces MC aggregation and degranulation, leading to the release of algogenic substances including 5-HT and HA, which result in localized cutaneous hyperalgesia. Labels: CGRP: Calcitonin gene-related peptide; SP: Substance P; MC: Mast cell; 5-HT: 5-Hydroxytryptamine hydrochloride; HA: Histamine; NA: Noradrenaline; AGMI: Acute gastric mucosal injury; SDH: Spinal dorsal horn; i.g.: Oral gavage; i.v.: Intravenous injection.