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Objective:To explore an ideal method for establishing a mouse model of chronic atrophic gastritis (CAG).Methods:CAG mouse models were established with five different modeling methods ( N-methyl- N′-nitro- N-nitrosoguanide (MNNG), sodium salicylate, sodium deoxycholate, Helicobacter pylori infection, and combinations of them) in BALB/c and C57 mice. The effect of each modeling method was evaluated by histological observation of gastric mucosa, plasma biochemical parameters, inflammatory response score, and the expression of anti-inflammatory factors. Results:The results of histological observation of gastric mucosa showed that all of the 5 methods could successfully establish CAG mouse models. In BALB/c mice, compared with the healthy control group, significant features of CAG accompanied with intestinal metaplasia was found in the model group established by combination of MNNG-free drinking, 2% sodium salicylate and 20 mmol sodium deoxycholate. From the results of serological detection, compared with the normal control group, the mRNA expression levels of related anti-inflammatory factors interleukin-2, interleukin-10, interleukin-13 and growth differentiation factor-15 of each model group decreased, which indicated that the mice of each CAG model group had different degrees of inflammation. The results of plasma biochemical parameters indicated that plasma gastrin of each group decreased and the ratio of pepsinogen Ⅰ and pepsinogen Ⅱ significantly dropped. The above results demonstrated that in BLAB/c mice, MNNG-free drinking, 2% sodium salicylate and 20 mmol sodium deoxycholate was better than other four modeling methods. For C57 mice, it was also found that simple chemical drug mutagenesis and Helicobacter pylori replication method both could successfully establish CAG models. No matter from pathological observation, relative expression of anti-inflammatory factors and analysis of plasma biochemical parameters, the effects of combination of the two methods was better. Conclusion:The CAG mouse model established by MNNG-free drinking, 2% sodium salicylate and 20 mmol sodium deoxycholate can provide a certain reference for the establishment and application of mouse model in CAG experiments in the future for pharmacological research.
RESUMEN
A 31-year-old male normotensive patient with aldosterone-producmg adenoma complained of thirst,polydipsia,polyuria,and periodical paraplegia.The diagnosis is raised by signs of hypokalemia.Despite the lack of hypertension,primary aldosteronism was confirmed by persistent hypokalemia,increased urinary potassium,increased urinary and plasma aldosterone levels and suppressed plasma rennin activity (PRA).The blood pressure profile was studied by ambulatory monitoring,and the mean blood pressure of 24h was normal and the circadian rhythm remained normal. Surgical removal of the histologically typical aldosterone-producing adenomas normalized the kalemia.The patient had a marked fall in blood pressure with mean values of 21/17 mm Hg ( diurnal and nocturnal blood pressure were 19/17 and 22/17 mm Hg respectively)and recovery of normal urinary and plasma aldosterone levels and PRA 6 weeks after surgery.This suggests that excess serum aldosterone induced relative hypertension in those patients whose blood pressure was spontaneously very low.Our observations call for primary hyperaldosteronism assay in patients with hypokalemia and renal potassium leakage.