The Role Of Gastrin And Somatostatin In Injury And Repair Of Gastric Mucosal

Objective:To investigate the role of gastrin and somatostatin in injury and repair of gastricmucosal by observing the pathological changes and comparing the Gas,SS andcaspase-3positive cell numbers of normal,injured,repaired and protected gastrictissues of ras model,and further explore the preventive and therapeutic effects ofrhein on gastric mucosal injury and relevant mechanisms.Methods:Forty adult female SD rats weighing200±20g were randomly divided into fourgroups (n=10per group): normal gastric mucosa group (control group), gastricmucosal injury group (injury group), rhein protection group (protection group) andrhein treatment group (repair group). All animals were fed for a one-week controlperiod. The injury group was administered BSA+LPS+CCl4to establish themodel, and the protection and repair groups were administered rhein by gavagebefore and after application of modeling reagents. The animals were sacrificed atweek10, and the gastric antrum was taken, fixed in4%paraformaldehyde solutionat4°C for24h, paraffin-embedded and sliced. HE staining was applied to observethe gastric pathological changes; immunohistochemical methods were used todisplay antral gastrin (Gas)-, somatostatin (SS)-, and caspase-3-positive cells; thenumber densities of these cells in each group were measured using stereologicalmethods. By the software SPSS statistics17.0, comparisons between groups for allparameters were performed using one-way ANOVA analysis and correlation analysiswas performed between parameters, with P<0.05being considered significant and P<0.01very significant.Results:1. Pathological observations and comparisons: In the control group, integrategastric mucosal epithelium, rare exfoliated cells in the stomach cavity surface andtightly arranged glands were observed, and no congestion and hemorrhage occurred. In the injury group, varying degrees of gastric glandular off or missing in the surfaceepithelium of local gastric mucosa, loosely arranged gastric glands, atrophied glandcells, some damaged and missed glands and hemorrhage of the mucosal layer wereobserved. Compared with the injury group, the gastric mucosal injury in theprotection and repair groups were alleviated (the difference between these twogroups was not significant), manifested by off or missing of gastric glands in thesurface epithelium of local gastric mucosa (less serious than that in the injury group),atrophy of gland cells and small mount of hemorrhage in the mucosal layer.2. Metrology: The immunohistochemical results showed that the expression ofgastrin-positive cells in the injury group significantly desreased compared with thecontrol group, while that in the protection and repair groups was lower than in thecontrol group, but higher than in the injury group; the expression of somatostatin-and caspase-3-positive cells in the injury group significantly increased comparedwith the control group, while that in the protection and repair groups was higher thanin the control group, but lower than in the injury group. By stereological analysis,the number densities of gastrin-positive cells in the injury, protection, repair andcontrol groups were1.884±0.030,2.355±0.008,2.268±0.010and3.250±0.067(×10-5μm-3), respectively, according which, that in the injury group decreasedcompared with the control group (P <0.05), and that in the protection and repairgroups increased compared with the injury group (P <0.05); the number densities ofSS-positive cells in the injury, protection, repair and control groups were1.976±0.014,1.559±0.031,1.653±0.050and1.353±0.034(×10-5μm-3), respectively,according which, there was an increase in the injury group compared with thecontrol group (P <0.05), and an decrease in the protection and repair groupscompared with the injury group (P <0.05); the number densities of caspase-3cells inthe injury, protection, repair and control groups were33.475±0.304,19.365±0.030,23.278±0.139and9.250±0.067(×10-5μm-3), respectively, according which, thatin the injury group had an increase compared with the control group (P <0.05), andan decrease in the protection and repair groups compared with the injury group (P<0.05).3. Correlation analysis: Changes in the number densities of Gas-and SS-positive cells were negatively correlated (r=0.911, P <0.01); changes in thenumber densities of Gas-positive cells and caspase-3positive protein expressionwere negatively correlated (r=0.960, P <0.01); changes in the number densities ofSS-positive cells and caspase-3positive protein expression were positivelycorrelated (r=0.982, P <0.01).Conclusions:1. BSA+LPS+CCl4can cause gastric mucosal injury and apoptosis.2. Rhein can alleviate and repair gastric mucosal injury and apoptosis caused byBSA+LPS+CCl4.3. Rhein can increase the number density of Gas-positive cells and reduce thenumber density of SS-positive cells in the injured rat gastric mucosa, and therefore,it may has protective and repairing effects on gastric mucosal injury by regulatingthe content of these two hormones to reduce apoptosis.