Ischemic stroke results in the diverse phathophysiologies including blood brain barrier (BBB) disruption, brain edema, neuronal cell death, and synaptic loss in brain. Vitamin C has known as the potent anti-oxidant having multiple functions in various organs, as well as in brain. Dehydroascorbic acid (DHA) as the oxidized form of ascorbic acid (AA) acts as a cellular protector against oxidative stress and easily enters into the brain compared to AA. To determine the role of DHA on edema formation, neuronal cell death, and synaptic dysfunction following cerebral ischemia, we investigated the infarct size of ischemic brain tissue and measured the expression of aquaporin 1 (AQP-1) as the water channel protein. We also examined the expression of claudin 5 for confirming the BBB breakdown, and the expression of bcl 2 associated X protein (Bax), caspase-3, inducible nitric oxide synthase (iNOS) for checking the effect of DHA on the neurotoxicity. Finally, we examined postsynaptic density protein-95 (PSD-95) expression to confirm the effect of DHA on synaptic dysfunction following ischemic stroke. Based on our findings, we propose that DHA might alleviate the pathogenesis of ischemic brain injury by attenuating edema, neuronal loss, and by improving synaptic connection.
Aquaporins ; Aquaporin 1 ; Ascorbic Acid ; bcl-2-Associated X Protein ; Blood-Brain Barrier ; Brain ; Brain Edema* ; Brain Injuries ; Brain Ischemia* ; Caspase 3 ; Cell Death ; Claudin-5 ; Dehydroascorbic Acid* ; Edema ; Neurons ; Nitric Oxide Synthase Type II ; Oxidative Stress ; Post-Synaptic Density ; Stroke

Aquaporins (AQPs) are expressed in myocardium and the implication of AQPs in myocardial water balance has been suggested. We investigated the expression patterns of AQP subtypes in normal myocardium and their changes in the process of edema formation and cardiac dysfunction following myocardial infarction (MI). Immunostaining demonstrated abundant expression of AQP1, AQP4, and AQP6 in normal mouse heart; AQP1 in blood vessels and cardiac myocytes, AQP4 exclusively on the intercalated discs between cardiac myocytes and AQP6 inside the myocytes. However, neither AQP7 nor AQP9 proteins were expressed in CD1 mouse myocardium. Echocardiography revealed that cardiac function was reduced at 1 week and recovered at 4 weeks after MI, whereas myocardial water content determined by wet-to-dry weight ratio increased at 1 week and rather reduced below the normal at 4 weeks. The expression of cardiac AQPs was up-regulated in MI-induced groups compared with sham-operated control group, but their time-dependent patterns were different. The time course of AQP4 expression coincided with that of myocardial edema and cardiac dysfunction following MI. However, expression of both AQP1 and AQP6 increased persistently up to 4 weeks. Our findings suggest a different role for cardiac AQPs in the formation and reabsorption of myocardial edema after MI.
Animals ; Aquaporin 1/metabolism ; Aquaporin 4/metabolism ; Aquaporin 6/metabolism ; Aquaporins/*metabolism ; Edema/pathology ; Immunohistochemistry ; Mice ; Muscle Cells/metabolism ; Myocardial Infarction/*metabolism/pathology/ultrasonography ; Myocardium/metabolism/pathology ; Time Factors

OBJECTIVETo investigate the expression of aquaporin (AQP)-1, 3, 8, 9 in human fetal membrane and their role in the human amniotic fluid circulation.

METHODSRT-PCR was employed for detection of the expressions of AQP-1, 3, 8, 9 mRNA in human amnion and chorion from 20 women with normal term pregnancy.

RESULTSAQP-1, 3, 8, 9 mRNA expression was detected in both human amnion and chorion, and no significant difference was found in their expression levels or between the amnion and chorion (P>0.05).

CONCLUSIONAQP-1, 3, 8, 9 can be associated with intramembranous transport and volume regulation of amniotic fluid.

Adult ; Amnion ; embryology ; metabolism ; Aquaporin 1 ; genetics ; Aquaporin 3 ; genetics ; Aquaporins ; genetics ; Chorion ; embryology ; metabolism ; Electrophoresis, Agar Gel ; Extraembryonic Membranes ; embryology ; metabolism ; Female ; Gene Expression Regulation, Developmental ; Humans ; Pregnancy ; Reverse Transcriptase Polymerase Chain Reaction

OBJECTIVETo investigate the expression of aquaporin 3, 4, and 8 in the colonic mucosa of rat models with slow transit constipation (STC).

METHODSSTC rat model was established by giving the rats the compound solution of diphenoxylate. Real time polymerase chain reaction (RT-PCR) was used to measure the expression of aquaporin mRNA in colonic mucosa of STC rat models (study group,n=16) and normal rats (control group,n=16). Gray scale ratio of aquaporin to β-action (internal reference) was used for quantification.

RESULTSRT-PCR revealed that the mean gray scale ratios of aquaporin 3 in the proximal colon of the study group and control group were 0.344 and 0.602 (P<0.05), and were 0.419 and 0.509 in the distal colon (P>0.05), respectively. The mean gray scale ratios of aquaporin 4 in the proximal and the distal colon were 0.764 and 0.759 in the study group (P>0.05), and were 0.776 and 0.736 in the control group (P>0.05), respectively. However, there was no expression of aquaporin 8 in the proximal and the distal colon in either the study group or the control groups.

CONCLUSIONSExpression of aquaporin 3 in the proximal colon of STC rat models is down-regulated, which regulates water absorption. There are no significant changes in the expressions of aquaporin 4 and 8.

Animals ; Aquaporin 3 ; metabolism ; Aquaporin 4 ; metabolism ; Aquaporins ; metabolism ; Colon ; metabolism ; Constipation ; metabolism ; Disease Models, Animal ; Female ; Intestinal Mucosa ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo determine if aquaporin1 (AQP1) and aquaporin5 (AQP5) are expressed in the alveolar capillary membrane in rats. Moreover, to investigate the alteration of AQP1 and AQP5 in acute injured lungs.

METHODSThe distribution of AQP1 and AQP5 in alveolar capillary membrane were investigated by immunohistochemistry and immunoelectron microscopy with affinity-purified antibodies to human AQP1 and AQP5. To study the possibility that alveolar capillary membrane AQP1 and AQP5 undergo altered regulation, we established a rat model using alveolar instillation of lipopolysaccharide (LPS).

RESULTSImmunolabelling showed AQP1 was stained primarily in the microvascular endotheli a of normal lungs, while AQP5 was expressed in type I pneumocytes. Immunohisto chemical analysis showed a significant decrease in the expression of AQP1 and AQP5 in injured lungs at 4h-48h after LPS instillation. AQP1 protein was resumed partly at 24h after LPS instillation and steroid administration, whereas AQP5 was unchanged.

CONCLUSIONThe decreased expressions of AQP1 and AQP5 in injured lungs suggest that both of them may play a role in abnormal fluid transportation.

Animals ; Aquaporin 1 ; Aquaporin 5 ; Aquaporins ; analysis ; Immunohistochemistry ; Lipopolysaccharides ; toxicity ; Lung ; metabolism ; Male ; Membrane Proteins ; Microscopy, Immunoelectron ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult ; metabolism ; pathology

BACKGROUND: Aquaporins (AQPs) are a family of water transporting proteins present in many mammalian epithelial and endothelial cell types. Among the AQPs, AQP3 is known to be a water/glycerol transporter expressed in human skin. OBJECTIVE: The relationship between the expression level of AQP3 and transpidermal water loss (TEWL) in the lesional and peri-lesional skin of psoriasis-affected patients, and skin hydration in the lesional and peri-lesional skin of psoriasis patients, was investigated. METHODS: The expression of AQP3 in psoriasis-affected and healthy control skin was determined using immunohistochemical and immunofluroscence staining. TEWL and skin hydration were measured using a Tewameter(R) TM210 (Courage & Khazaka, Cologne, Germany) and a Corneometer(R) CM 820 (Courage & Khazaka), respectively. RESULTS: AQP3 was mainly expressed in the plasma membrane of stratum corneum and the stratum spinosum in normal epidermis. Unlike the normal epidermis, AQP3 showed decreased expression in the lesional and peri-lesional epidermis of psoriasis. TEWL was increased, and skin hydration was decreased, in the lesional and peri-lesional skin of psoriasis patients, compared with the healthy control sample. CONCLUSION: Although various factors contribute to reduced skin hydration in the lesional and peri-lesional skin of psoriasis, AQP3 appears to be a key factor in the skin dehydration of psoriasis-affected skin.
Aquaporin 3 ; Aquaporins ; Cell Membrane ; Dehydration ; Endothelial Cells ; Epidermis ; Humans ; Proteins ; Psoriasis ; Skin ; Water Loss, Insensible

OBJECTIVETo explore the relationship between Pi-Wei Damp-Heat Syndrome (PWDHS) with expression of aquaporin (AQP) 3,4 gene in gastric mucosa and the effects of Qingre Huashi Recipe (QHR) on the expression.

METHODSSixty-eight patients with chronic superficial gastritis were differentiated into Pi-Wei Damp-Heat Syndrome group (PWDHS, n = 53, 19 cases with predominant Dampness, 14 cases with predominant Heat, 20 cases with Dampness equal to Heat) and Pi deficiency Syndrome group (PDS, n = 15). The PWDHS were treated with QHR. The expression of AQP 3,4 gene in the two groups were determined by fluorescence quantitative polymerase chain reaction (FQ-PCR).

RESULTSExpression of AQP 3 gene in PWDHS was higher than that in PDS and the healthy group, but the difference showed no statistical significance. Expression of AQP 4 gene in PWDHS was obvious higher than that in PDS and the healthy group (P <0.05 or P <0.01), but the difference of AQP 4 gene expression between PDS and the healthy group was insignificant. Comparison among various sub-types of PWDHS showed that the AQP 4 gene expression in the predominant dampness > dampness equal to heat> predominant heat. AQP 3,4 gene expression in PWDHS was significantly decreased after QHR treatment, especially in the cases with predominant dampness syndrome (P <0.01), approaching that in the healthy group and PDS.

CONCLUSIONAbnormal expression of AQP 3,4 gene may be one of the possible mechanisms of PWDHS pathogenesis, Chinese herbs could influence AQP 3,4 gene expression to play a key role in treatment.

Adult ; Aquaporin 3 ; Aquaporin 4 ; Aquaporins ; biosynthesis ; genetics ; Diagnosis, Differential ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Gastric Mucosa ; metabolism ; Gastritis ; drug therapy ; genetics ; metabolism ; Humans ; Male ; Medicine, Chinese Traditional ; Phytotherapy

No abstract available.
Aquaporins* ; Kidney*

BACKGROUND: The present study was aimed at investigating whether there is a mechanism exerted by endogenous nitric oxide(NO) in the regulation of aquaporin(AQP) water channels in the kidney. METHODS: Male Sprague-Dawley rats were treated with N(G)-nitro-L-arginine methyl ester(L-NAME, 40 mg/L drinking water) to inhibit the endogenous generation of nitric oxide. Four weeks later, total abundance and shuttling of AQP2 proteins were determined in different regions of the kidney. RESULTS: Chronic inhibition of NO synthesis increased the expression of AQP2 channels in cortex, outer medulla, and inner medulla of the kidney. The AQP2 shuttling was not significantly altered, as evidenced by an unaltered ratio of AQP2 expression in the membrane fraction versus that in the cytoplasmic fraction. CONCLUSION: It is suggested that endogenous NO activity plays a tonic inhibitory role in the expression of AQP2 channels in the kidney.
Animals ; Aquaporin 2* ; Aquaporins* ; Cytoplasm ; Drinking ; Humans ; Kidney* ; Male ; Membranes ; Nitric Oxide* ; Rats* ; Rats, Sprague-Dawley

BACKGROUND:The present study aimed to determine whether there is a regulatory mechanism exerted by endogenous nitric oxide (NO) in the regulation of aquaporin (AQP) water channels in the kidney. METHODS:Male Sprague-Dawley rats were used. They were divided into 4 groups: 1) L-NAME group was treated with N(G)-nitro-L-arginine methyl ester (L-NAME, 100 mg/L drinking water) for 1 week, 2) indomethacin group was treated with indomethacin (5 mg/kg, twice a day, i.p.) for 2 days, 3) L-NAME/ indomethacin group was treated with L-NAME for 1 week in which indomethacin was cotreated for the last two days, and 4) control group was kept untreated. The abundance of AQP2 and AQP3 proteins was determined in the inner medulla of the kidney. RESULTS:The expression of AQP2 and AQP3 proteins was significantly decreased by indomethacin. L-NAME abolished the indomethacin-induced decreases of AQP channels, although it did not significantly affect the expression of AQP channels by itself. CONCLUSION:These results suggest that endogenous NO system, when stimulated, may downregulate the expression of AQP2 and AQP3 channels in the kidney.
Animals ; Aquaporin 3 ; Aquaporins* ; Down-Regulation* ; Drinking ; Indomethacin ; Kidney ; NG-Nitroarginine Methyl Ester ; Nitric Oxide* ; Rats* ; Rats, Sprague-Dawley