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Objective To investigate the age-associated changes of ultrastructure,mRNA and protein expressions of H+-K+-ATPase in elderly gastric parietal cell. Methods Fifty patients with relative normal stomach without gastroduodenal diseases were enrolled,including younger group (aged 20-59 years,n=19) and elderly group (aged≥60 years,n=31).Furthermore,the elderly group was divided into 3 subgroups:60-69 years old (n =11 ),70-79 years old (n=10 ),above 80 years old (n =10).The ultrastructure of gastric parietal cell was observed under electron microscope.The expression of H+-K+-ATPase α subunit mRNA and H+-K+-ATPase β subunit protein were assessed by quantitative real-time PCR and Western-blot,respectively.The ageing-associated changes of all these data were respectively compared. Results No significant difference was showed in the morphology of gastric parietal cell and acid-secretion-associated organelles among all the groups.The average ratio Am to Ac (Am means the area of mitochondria,Ac means the area of cytoplasm) of gastric parietal cell and the average At to Ac ratio (At means the area of secretory canaliculi and tubulovesicular system )between younger group and elderly group had no significant difference[(48.4±7.5) ％ vs.(50.6±7.6) ％,t=-0.775,P=0.444; (13.8±4.1) ％ vs.(12.2±4.7) ％,t=0.984,P=0.332].Meanwhile,there were no distinctions in the expression of H+-K+ -ATPase α subunit mRNA and H+-K+-ATPase protein among all elderly subgroups(F=1.522,2.32,P=0.24,0.114).However,the mRNA expression of H+-K+-ATPase a subunit was higher in the elderly group than in the younger group(t=-3.682,P=0.001).Furthermore,the expression of H+ -K+ -ATPase protein in the elderly group was increased as compared with younger group(t=-3.389,P=0.004). Conclusions Acidsecretion-associated organelles of human gastric parietal cell have no degeneration and the expression of H + -K+-ATPase is in trend of increase with aging,indicating that healthy elderly people have the basis of ultrastructure and molecular biology to maintain well function of acid secretion.
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Objective To investigate the inhibitory mechanism of rabeprazole on acid secretion of parietal cells in rats. Methods Seventy two Spraque-Dawley rats were divided into control group(normal saline), low dose of rabeprazole group (rabeprazole 10 mg/kg) and high dose of rabeprazole group (rabeprazole 20 mg/kg) with 24 each. Four rats in each group were treated at 1 h, 2 h, 4 h, 6 h, 12 h and 24 h, respectively, pH value and activity of H+-K+-ATPase were tested by NaOH titrimetric method and chromatometry, respectively. The changes of ultrastructure of parietal cells were observed by electron microscope. Results Compared with control group(1.97±0.30), pH value in low (3.37± 0.97)and high (5.96±0.26)dose groups were significantly increased(P<0.01), and the activity of H+-K+-ATPase was inhibited obviously at 1 h after administration(3.28±0. 41 vs 1.47±0.27 and 0.92±0.07, P<0.05). Those differences could be found even at 12 h(P<0.01). The ultrastructural changes of parietal cells were consistent with the increase of pH value and decreased activity of H+-K+-ATPase. The significant difference was found in acid depression and excellent time between low and high dose of rabeprazole groups. Conclnsions The uhrastructural changes of parietal cells and the activity of H+-K+-ATPase can accurately reflect the acid secretion in rats. Rabeprazole has powerful and rapid effects in inhibiting acid secretion which correlates with the dosage.
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Objective To study the properties of K~ +-ion channel of rat parietal cells, and to approach its effects on physiological and pathological process. Method Parietal cells were isolated. Electrophysiological records of K~ +-ion channels were made through whole cell's patch clamp technique, and the properties of the channels were analyzed. Results 10mM tetraethylammonium chloride may partially block the outwardly depolarized K~ +-ion channel current. While 10mM tetraethylammonium acetate, 10mM barium chloride or 10mM barium acetate may increases the outwardly depolarized K~ +-ion channel current. Conclusion The whole cell K~ +-ion channel current of rat parietal cells showed voltage sensitive. The current-voltage relations of whole cell potassium channels of rat parietal cells are both outwardly and inwardly rectified.
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Objective To investigate the effect of H.pylori infection and eradication on gastric parietal cell and H + K +ATPase mRNA expression in a murine model. Methods Twenty 7 week old SPF BALB/C mice (10 males and 10 females) each were fed by H.pylori strain (Sydney Strain 1,SS1) at a dose of 0.4 ml (10 9CFU) per day for consecutive 5 days. Two months after infection of H. pylori, all mice were divided into two groups, the eradication group (10 mice) and the infection group (10 mice). Mice in the eradication group were administered clarithromycin ( 13.5 mg?kg -1 ?d -1 ) twice per day for one week (one mouse was died).Meanwhile, mice in the infection group were given the same amount placebo. All mice were killed at one month after the administration.The gastric mucosa was removed for rapid urease testing (RUT) and Giemsa stainning. The expression of H + K +ATPase mRNA was detected by RT PCR. Morphological changes in parietal cells were assessed by electron microscope. Results The animals in infection group were 100% infected by H.pylori, and RUT and Giemsa staining were all positive. Meanwhile , all but one mouse in the eradcation group were negative to RUT and Giemsa staining. In the infection group, the average ratio A C to A T (A C means the area of the canaliculi, A T means the area of the parietal cells ) was ( 2.20 ? 0.06 )/10 4, significant lower than that in the eradication group [(3.20 ? 0.06 )/10 4, P
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The aim of this study was to demonstrate the effect of acid inhibitor on the function and ultrastructure of gastric parietal cells in rats under immersion and restraint stress. Thirty two male SD rats were randomly divided into control, stress, omeprazole and cimetidine treated groups. The gastric mucosal ulcer index (UI) and gastric juice pH were measured. The ultrastructural changes of parietal cells were observed by transmission electronic microscopy (TEM). The UI was decreased and the pH value was increased obviously in omeprazole and cimetidine treated groups compared with stress group ( P
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AIM: To evaluate the dynamic changes of the function and ultrastructure of gastric parietal cells under stress and their relation with acute gastric mucosal lesions. METHODS: Thirty-two male SD rats were randomly divided into four groups, which were control group and 1,2,4 h groups under water restraint stress (WRS). The gastric fluid pH value and gastric mucosal ulcer index(UI) were measured. The ultrastructural changes of parietal cells were observed by transmission electronic microscopy (TEM). RESULTS: The study demonstrated that gastric acid secretion increased and gastric fluid pH value decreased gradually and significantly under WRS compared with control group( P
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The aim of the study was to demonstrate the influence of immersion and restraint stress on the ultrastructural changes in gastric acid barrier and parietal cells in rats. Twenty rats were randomly divided into control and stress groups. The gastric mucosal ulcer index was measured. The ultrastructural changes in parietal cells, epithelial cells, epithelial cell junctions, and basal lamina were observed by transmission electronic microscopy. Stress could induce gastric mucosal damage obviously. Parietal cells in a resting state in control group but became active in stress groups with plenty of mitochromosomes and secreting cysts. The cell membrane of epithelium on the luminal surface were were injured with the preservation of tight junction and basal lamina. The results indicated that the stress induced acid secretion of parietal cells, which destroys the luminal surface of the epithelium. It thus suggests the significance of epithelial cell membrane damage in the development of stress ulcer.