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Objective To study the effect of ganoderma lucidum polysaccharides on T cell subsets and AQP1, AQP3 expression of bladder cancer T24 cell line bearing mice.Methods 60 BALB/C nude mice were selection as experimental animals, bladder tumor bearing animal models were made by bladder cancer T24 cells subcutaneous injection, and were randomly divided into control group, cisplatin group, ganoderma lucidum polysaccharides and cisplatin group, cisplatin group given 25 mg/kgcisplatin intraperitoneal injection, cisplatin combined ganoderma lucidum polysaccharide group given 200 mg/kg ganoderma lucidum polysaccharide lavage, 25 mg/kg cisplatin intraperitoneal injection, the control group given quite a volume normal saline lavage.Then tumor volume and weight, peripheral blood T cell subsets and AQP1, AQP3, Caspase-3, Bax mRNA content in tumor tissue were determined.Results Cisplatin group, cisplatin combined ganoderma lucidum polysaccharide tumor volume and mass were significantly lower than the control group (P<0.05), cisplatin and ganoderma lucidum polysaccharide tumor volume and mass were significantly lower than that cisplatin group ( P<0.05 ); Cisplatin group, cisplatin combined ganoderma lucidum polysaccharides group CD4 + T cells, CD8 +T cells , CD4 +/CD8 + were significantly higher than that of control group (P<0.05), cisplatin combined ganoderma lucidum polysaccharide group CD4 +T cells, CD4 +/CD8 +were significantly higher than that of cisplatin group (P<0.05); Cisplatin group, cisplatin combined ganoderma lucidum polysaccharide group mices tumor tissues Bax, Caspase 3 mRNA content were significantly lower than the control group (P<0.05), cisplatin combined ganoderma lucidum polysaccharide group Bax,caspase 3 mRNA content were significantly lower than that of cisplatin group (P<0.05); Cisplatin group, cisplatin combined ganoderma lucidum polysaccharide group mice tumor tissue AQP1, AQP3 mRNA content were significantly lower than the control group (P<0.05); Cisplatin combined ganoderma lucidum polysaccharide group AQP1, AQP3 mRNA content were significantly lower than cisplatin group (P<0.05 ). Conclusion ganoderma lucidum polysaccharide can inhibit tumor growth and enhance cellular immune function of bladder cancer T24 cell line bearing mice, and adjust the expression of pro-apoptotic genes, AQP1 and AQP3.
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La hormona antidiurética arginina vasopresina (AVP) es liberada de la hipófisis, y regula la reabsorción de agua en las células principales del túbulo colector renal. La unión de la AVP al receptor tipo 2 de la AVP en la membrana basolateral induce la translocación de los canales acuosos de la acuaporina-2 hacia la membrana apical de las células principales de los túbulos colectores, induciendo la permeabilidad al agua de la membrana. Lo anterior da como resultado la reabsorción de agua en el túbulo colector de la nefrona, bajo la influencia de un gradiente osmótico. La diabetes insípida nefrogénica es causada por la resistencia parcial o total al efecto de la AVP. La diabetes insípida nefrogénica congénita es una alteración asociada con mutaciones en los genes AVPR2 o AQP2, ocasionando la incapacidad del paciente para concentrar la orina. La diabetes insípida nefrogénica adquirida o secundaria puede ser causada por desbalances electrolíticos (hipercalcemia, hipokalemia), enfermedades renales o extrarrenales y fármacos (toxicidad por litio). En este artículo se revisan las causas, manifestaciones clínicas, diagnóstico y tratamiento de los pacientes con diabetes insípida nefrogénica. También, con base en la comprensión de los mecanismos íntimos de la alteración, se exploran nuevas estrategias terapéuticas.
The anti-diuretic hormone arginine-vasopressin (AVP) is released from the pituitary and regulates water reabsorption in the principal cells of the kidney collecting duct. Binding of AVP to the arginine-vasopressin receptor type-2 in the basolateral membrane leads to translocation of aquaporin-2 water channels to the apical membrane of the principal cells of the collecting duct, inducing water permeability of the membrane. This results in water reabsorption in the collecting duct of the nephron following an osmotic gradient. Nephrogenic diabetes insipidus is caused by partial or complete renal resistance to the effects of AVP. Congenital nephrogenic diabetes insipidus is a disorder associated with mutations in either the AVPR2 or AQP2 gene, causing the inability of patients to concentrate their urine. Acquired nephrogenic diabetes insipidus can be caused by electrolyte imbalances (e.g., hypercalcemia, hypokalemia), renal/extra-renal diseases and drugs (e.g., lithium toxicity). This article reviews the causes, clinical manifestations, diagnosis and treatment of patients with nephrogenic diabetes insipidus. Based on more in-depth mechanistic understanding, new therapeutic strategies are current being explored.
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Objective To investigate the role of AQP2 and Na +-K +-ATPase in the pathogenesis of kidney injury with multiple organ dysfunction syndrome,and try to find the express characteristics of them.Methods A total of 72 healthy rats were randomly (random number) divided into two groups:control group (n =24) and Lipopolysaccharide group (n =48).The Lipopolysaccharide group rats were injected with 5 mg/kg lipopolysaccharide at the beginning while the control group was 0.9％ sodium chloride.After the model was succeeded,the rats were put to death at 6 h,12 h,24 h,2 days,3 days and 5 days equally.The urine and blood were collected.Blood were used biochemical tests to check.kidney AQP2 protein and mRNA expression level in the organization were applied the immune organized and RT-PCR technique to detect.Applied kit for determining the content and activity of sodium/potassium-atpase.Results The volume of urine in LPS group decrease quickly at 12 h and 24 h,but increased after 2 days.Urea nitrogen and creatinine increased gradually,and peaked at 48 h,after then gradually decline.AQP2 mRNA and protein expression decreased,and minimize at 48 h.The content of Na+-K+-ATP ase has no obvious difference,but the activity significantly decreased at the beginning,then increased gradually,but it was still lower than the control group.Conclusions In renal injury rats model with multiple organ dysfunction syndrome,AQP2 is the structure of renal reabsorption function,while Na +-K +-ATPase directly involved in or indirectly reflected the state of kidney energy metabolism.Recovery of AQP2 protein and energy metabolism,before the rat kidney function improved.
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Objective To testify the lung injury induced by cardiopulmonary bypass(CPB) in canine model and observe the influence of CPB on the aquaporin-1 ( AQP1 ) mRNA expression in canine lung. Methods 8 mongrel dogs were used to perform the cardiopulmonary bypass. The hearts arrested for 90 minutes with mild hypothermia and rebeated for 6 hours. The hemodynamics, the ratio of lung dry weight and wet weight, the plasmic osmotic pressure, and the characteristics of light and fine structure were analyzed. The retro-transcription polyase chain reaction ( RT-PCR ) was used to measure the expression of AQP1 mRNA during the CPB. Results The hemodynamic data were stable in different time point during the CPB (P ＞0.05 ). The ratio of lung dry weight and wet weight was getting lower ( P ＜0.001) and the plasmic osmotic pressure was getting higher due to the prolongation of the CPB time and reperfusion time ( P ＜0.01). The light and electron microscopy showed the prominent aggregation of the white blood cell, severe interstitial edema and mild tear of respiratory membrane after 3 hour and 6-hour rebeat. AQP1 mRNA expression in lung was downregulated, 78.4% after 3-hour reperfusion and 55.5% after 6-hour reperfusion respectively, comparing to the level before CPB. Conclusion We recognize that the lung injury and lung edema were severe following 3-hour and 6-hour rebeat in CPB and hypothesize that the down-regulation of lung AQP1 mRNA expression may be a sign of pulmonary interstitial capillary injury induced by CPB.
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The aquaporins (AQPs) are small, integral-membrane proteins which selectively transport water across cell plasma membranes. AQPs are over-expressed in tumor cells of different origins, particularly aggressive tumors. AQPs-expressing cancer cells show enhanced migration in vitro and greater local tumor invasion, tumor cell extrava-sations, and metastases in vivo. AQPs inhibition will provide a help for tumor therapy.
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Objective To study the expression and regulation characteristics of aquaporin water channel(AQP) of cerebuller metastatic tumor and brain tissue surrounding tumor and to understand the role of abnormal expression of AQP in formation and elimination of brain edema.Methods The tumor tissue specimens from five lung adencarcinoma brain metastasis cases after surgical resection were accessed.The total RNA was extracted,and RT-PCR,immunohistochemical staining were progressed to study the expression and regulation characteristics of AQP.The average gray values of near and far regions from tumor tissue were measured with HPIAS-1000 cells measuring procedure to compare actual expression quantity of AQP.Results AQP4 had a high expression in the peritumoral brain tissue and no expression in the center of brain metastasis tumor organization.The AQP4 staining was junior in the more distant region from tumor and it added significantly in the region close to the tumor tissue.Stained AQP1 was not found in cerebullar metastatic tumor and peritumoral brain microvascular endothelial cells.Conclusion The expression of AQP4 is increased significantly in the region next to the cerebullar metastatic tumor tightly.It is probably related to the formation of peritumoral brain edema.The negative expression of AQP1 might not be conducive to the removal of edema in the interspace of nerve cells.
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The salivary glands produce 1.5 l of fluid per day. As in other organs, the general paradigm in the salivary glands is that water movement occurs secondary to osmotic driving forces created by active salt transport. Therefore, high water permeability in salivary glands is expected to need a variety of aquaporin (AQP), a water channel. Although four AQPs have been known to reside in salivary glands, the precise location and roles of AQPs have been not well examined. This study is aimed to investigate the distribution of AQPs in 3 major salivary glands and their changes after cholinergic stimulation using immunohistochemical study in Sprague Dawley rats weighing 300 g under pentobarbital sodium anesthesia. AQP1 was localized in the endothelial cells of all salivary capillary vessels and the myoepithelial cells. AQP4 was demonstrated in the epithelium of the excretory ductal cells of all salivary glands. AQP5 and 8 were abundantly present in the basolateral membrane and apical membranes of the serous acini including intercellular secretory canaliculi, whereas AQP5 was weakly present in mucous acini. In addition, AQP5 was found in the epithelium of the intercalated and striated ducts. Upon stimulation of carbachol (10 micro gram/kg, I.P). AQP5 and 8 tended to translocate from basolateral membrane to the apical membrane, appearing as clusters of dots. These results suggest that AQP5 and 8 are the candidate molecules responsible for the water movement in salivary acinar cells.