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1.
Journal of Gorgan University of Medical Sciences. 2012; 14 (1): 1-9
in Persian | IMEMR | ID: emr-163149

ABSTRACT

The role of ion channels and particularly cationic channels in the pathogenesis of various diseases are being considered carefully. The diabetes mellitus is a common disease which is initiated by ion channel disturbances. This study was done to determine the characteristics of hepatocyte rough endoplasmic reticulum single cationic channel in Streptozocin-induced diabetic rats. This experimental study was done on 10 male adult Wistar rats and animals were randomly allocaied into diabetic and control groups. Diabetes induced by STZ [65 mg/kg/bw] intraperitounally. Rough endoplasmic reticulum vesicles were extracted following rat liver excision, homogenization and ultracentrifuging. The bilayer membrane formation was prepared by painting phosphatidylcholine on 250 micro M aperture in between Cis and Trans sides. The RER vesicles incorporation was performed through gentle and delicate touch of membrane using a dentistry needle. The Pclamp9 software was used for ion channel activity characteristic analysis. The cationic channel current amplitude did not change significantly in voltages more than+3o mV but their open probability [Po] decreased in diabetic group [P<0.05]. More severe changes in channel activity were seen in potentials less than the reverse potential. In addition to significant increase of channel Po [P<0.05], also, the channel unitary currents were significantly decreased [P<0.05]. The mean current amplitude and channel open probability in voltage+40 mV were 17 +/- 2.14 pA and 0.68 +/- 0.01 in control group respectively, whereas, the values of these parameters reached to 18.5 +/- 2.5 and 0.26 +/- 0.03, respectively. In voltage-10 mV, the values of mean current amplitude and Po were-22.3 +/- 2.14 pA and<0.1 in control group, respectively but the values changed to-13.1 +/- 0.08 and 0.62 +/- 0.03 in diabetic group. It seems that RER cationic channel is involved in metabolic changes which cause by diabetes mellitus and this disease can cause probably a channel gating kinetic and behavior change by inducing metabolic stresses


Subject(s)
Animals , Male , Hepatocytes/cytology , Hepatocytes/pathology , Diabetes Mellitus, Experimental , Rats, Wistar
2.
Journal of Medicinal Plants. 2009; 8 (29): 123-130
in Persian | IMEMR | ID: emr-91809

ABSTRACT

It has been clearly documented that Elaeagnus angustifolia [E.A.] have variety of medicinal uses including anti - ulcerogenic activity. Our recent study demonstrates that intragastric administration of E.A. blocked the carbachol - induced gastric acid secretion, completely. The aim of this work therefore is to evaluate the role of oral administration of E.A. on carbachol - induced gastric acid secretion in order to compare with intragastric effect of the drug. We also hypothesized that E.A. fruit might be involved in control of basal acid secretion and juice volume. To address this question, we investigated the oral effect of E.A. fruit extract on basal acid secretion on pylorous - ligated conscious rats. In this study we used pylorus ligation method. Briefly, animals were anesthetized and two cannulas were introduced into the stomach through esophagus to wash the stomach and pylorousdodenal junction to collect the stomach juice. Carbachol was infused into jugular vein and gastric juice was collected in 10 - min periods to titrate with NaOH 0.01 N. To concider the effect of the E.A. extraction on basal acid secretion, all experiments were performed in conscious rats who received the E.A. extract or saline 1.5 hours before pylorus-ligation. Ligation of pylorus was performed under brief ether anesthetized. Two and half hours after treatment, the stomach was removed, juice volume was measured and acid output was determined as above. Statistical analysis was performed by analysis of variance and subsequent tukey test. Our results showed that the E.A. fruit extract dose dependently decreased the carbachol - induced gastric acid secretion. Stimulated acid secretion was suppressed%52 +/- 4 at a dose 600 mg/kg and this inhibitory effect persisted up to the end of experiments.Oral administration of E.A. extraction in pylorus ligated conscious rats showed that the drug significantly stimulated gastric acid secretion and juice volume at a dose 1300 mg/kg within 1 hour, but there was no effect at lower doses. These results suggest that E.A. fruit has an anti-secretory action on cholinergic stimulated acid secretion by oral administration. This effect is less than the intragastric administration of the drug [% 81 +/- 4 inhibition]. It is likely that the inhibitory effect is mediated by cholinergic nervous system and/or non-neuronal membranes. We also suggest that the oral E.A. extract has no effect on basal acid secretion at lower doses


Subject(s)
Animals, Laboratory , Gastric Acid/metabolism , Consciousness , Rats , Administration, Oral , Medicine, Traditional , Carbachol
3.
Journal of Medicinal Plants. 2008; 7 (27): 82-91
in Persian | IMEMR | ID: emr-100345

ABSTRACT

It has been clearly documented that Elaegnaceae have a variety of medicinal uses including anti-ulcerogenic activity. We therefore hypothesized that Elaeagnus angustifulia L. [E. A.] fruit might be involved in the control of stimulated gastric acid secretion. To address this question, we investigated the pharmacological effect of the E. A. fruit extract on carbachol-induced acid secretion in a pylorus-ligated rat. In this study we used pylorus ligation method. Briefly, animals were anesthetized and two cannulas were introduced into the stomach through esophagus to inject drug and pylorododenal junction to collect the stomach juice. Carbachol or histamine was infused into jugular vein and gastric juice was collected in 10-min periods to titrate with NaOH 0.01 N. Our results showed that the E. A. fruit extract dose and time dependently decreased the carbachol- [but not histamine-] stimulated gastric acid secretion when it administered at increased steady level [at 30 minute] of carbachole time-course curve. Stimulated acid secretion was completely suppressed at a dose 600 mg/kg 30 min after drug administration and this inhibitory effect persisted up to the end of experiments [100 min]. Using E.A. fruit extract simultaneously with carbachol infusion had no effect on acid secretion. These results suggested that E.A. fruit has a pH-dependent anti-secretory action on cholinergic-stimulated gastric acid secretion by intragastric administration. It is likely that the inhibitory effect is mediated by cholinergic nervous system and/or non-neuronal membranes


Subject(s)
Animals, Laboratory , Gastric Acid/metabolism , Pylorus/surgery , Rats , Medicine, Traditional , Cholinergic Antagonists , Ligation , Models, Animal
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