1.A variant of ornithine aminotransferase from mouse small intestine.
Seong Nam LIM ; Hye Won RHO ; Jin Woo PARK ; Eun Chung JHEE ; Jong Suk KIM ; Hyung Rho KIM
Experimental & Molecular Medicine 1998;30(3):131-135
The ornithine aminotransferase (OAT) activity of mouse was found to be highest in the small intestine. The mitochondrial OAT from mouse small intestine was purified to homogeneity by the procedures including heart treatment, ammonium sulfate fractionation, octyl-Sepharose chromatography, and Sephadex G-150 gel filtration. Comparing to the amino acid sequence of mouse hepatic OAT, six N-terminal amino acid residues have been deleted in intestinal OAT. However, the subsequent sequence was identical with that of hepatic OAT. The molecular weights of both intestinal and hepatic OAT were estimated as 46 kDa by SDS-gel electrophoresis and as 92 kDa by gel filtration, indicating that both native OATs are dimeric. Biochemical properties of intestinal OAT, such as molecular weight, pH optimum and K(m) values for L-ornithine and alpha-ketoglutarate, were similar to those of hepatic OAT. However, intestinal OAT was more labile than hepatic OAT to tryptic digestion.
Amino Acid Sequence
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Animal
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Intestine, Small/enzymology*
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Liver/enzymology
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Male
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Mice
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Mice, Inbred ICR
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Molecular Sequence Data
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Molecular Weight
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Ornithine-Oxo-Acid Transaminase/metabolism*
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Ornithine-Oxo-Acid Transaminase/isolation & purification
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Ornithine-Oxo-Acid Transaminase/genetics*
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Tissue Distribution
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Trypsi
2.Effect of hypertonic versus isotonic saline resuscitation on heme oxygenase-1 expression in visceral organs following hemorrhagic shock in rats.
Yuan Qiang LU ; Lin Hui GU ; Jiu Kun JIANG ; Han Zhou MOU
Biomedical and Environmental Sciences 2013;26(8):684-688
To compare the early effects of hypertonic and isotonic saline resuscitation on heme oxygenase-1 (HO-1) expression in organs of rats with hemorrhagic shock. Rats were randomly divided into hypertonic saline resuscitation (HTS), normal saline resuscitation (NS) and sham groups. HO-1 mRNA, protein expression and apoptosis were evaluated in organs. In the HTS group, significant difference was noted in HO-1 protein in small intestinal mucosa and liver compared with the NS and sham groups, and in HO-1 mRNA in liver and kidney compared with the sham group. The apoptosis of small intestinal mucosa, liver, heart, and lung was significantly lower in the HTS group than that in the NS group. In this study, small volume resuscitation with HTS can efficiently up-regulate the expression level of HO-1 in small intestinal mucosa and liver, which may be one of the mechanisms alleviating organ damage.
Animals
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Base Sequence
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Blood Pressure
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DNA Primers
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Gene Expression Regulation, Enzymologic
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drug effects
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Heme Oxygenase-1
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metabolism
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Intestine, Small
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enzymology
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Kidney
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enzymology
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Liver
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enzymology
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RNA, Messenger
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genetics
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Rats
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Resuscitation
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methods
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Reverse Transcriptase Polymerase Chain Reaction
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Saline Solution, Hypertonic
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pharmacology
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Shock, Hemorrhagic
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enzymology
3.Inhibitory effects of saponins from Tribulus terrestris on alpha-glucosidase in small intestines of rats.
Su-jun ZHANG ; Wei-jing QU ; Shu-yun ZHONG
China Journal of Chinese Materia Medica 2006;31(11):910-913
OBJECTIVETo determine the effects of saponins from Tribulus terrestris (STT) on small intestinal a-glucosidase and postprandial blood glucose levels in rats.
METHODThe inhibitory effects of STT on a-glucosidase extracted from small intestines in rats were carried out in vitro. The blood glucose levels were measured after 60 min when sucrose (2 g x kg(-1)) or glucose (2 g x kg(-1)) was administered orally with STT (100 mg x kg(-1)). After treated with STT (100 mg x kg(-1)) for 14 d, the activities of a-glucosidase were determined daily, as well as the postprandial blood glucose levels after oraly administered sucrose (2 g x kg(-1)).
RESULTSTT at concentrations of 0.1, 1 and 10 mg x mL(-1) reduced significantly the activities of alpha-glucosidase with inhibitory rates of (20.83 +/- 1.66)%, (43.73 +/- 2.39)% and (52.62 +/- 2.69)%, respectively. In facts STT (100 mg x kg(-1)) considerably decreased the blood glucose levels which was 52.61% of that of the control in rats co-administered orally with sucrose (2 g x kg(-1)). However, it showed no such effect on the rats co-administered orally with glucose (2 g x kg(-1)). After orally administered of STT for 14 d, the activity of alpha-glucosidase was significantly reduced (P < 0.05) to (58.17 +/- 3.24)% of that those in control. Meanwhile, The rats were oral administered with sucrose, the increase of postprandial blood glucose levels were (69.50 +/- 4.28)% of that in control 60 min later ( P < 0.05).
CONCLUSIONIt was through inhibiting the activity of a-glucosidase in small intestines that STT significantly retarded the increase in postprandial blood glucose levels in rats.
Animals ; Blood Glucose ; metabolism ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; Intestine, Small ; enzymology ; Male ; Plants, Medicinal ; chemistry ; Postprandial Period ; Rats ; Rats, Sprague-Dawley ; Saponins ; isolation & purification ; pharmacology ; Tribulus ; chemistry ; alpha-Glucosidases ; metabolism
4.Difficult Establishment of a Chronic Nonsteroidal Anti-inflammatory Drugs Induced Gastric Inflammation Rat Model due to Gastric Adaptation and Small Bowel Damage.
Byoung Hwan LEE ; Nayoung KIM ; Ryoung Hee NAM ; Ju Yup LEE ; Hye Seung LEE ; Chang Hee LEE ; Ji Hyun PARK ; Dong Ho LEE
The Korean Journal of Gastroenterology 2014;63(6):341-347
BACKGROUND/AIMS: The prevalence of peptic ulcer disease has not decreased mainly due to an increase in the use of NSAIDs. This study was conducted in order to determine whether a chronic NSAID-induced gastric inflammation model could be established by repeated administration of NSAID. METHODS: Indomethacin (10 mg/kg) was administered once per week for six weeks in 8- and 26-week rats and animals were sacrificed every week after administration. Gross ulcer index, histologic damage index, myeloperoxidase (MPO) activity, and mucus (glucosamine) levels were measured. Small bowel damage was also evaluated. RESULTS: Gross gastric damage index showed a peak level at three weeks and then decreased slowly in the 26-week indomethacin group. Gastric mucosal glucosamine level increased in both the 8-week (p=0.038) and 26-week groups (p=0.007). In addition, gastric mucosal MPO level decreased in the 8-week group (p=0.018) but did not show a decrease in the 26-week group. Small bowel damage began to occur at three weeks during the schedule and eight of 36 rats (22.2%) died due to perforation or peritonitis of the small bowel in the 8- and 26-week indomethacin groups, respectively. CONCLUSIONS: Due to gastric adaptation and small bowel damage, repeated administration of NSAID to experimental animals may not be an adequate method for establishment of the chronic gastric inflammation model.
Animals
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Anti-Inflammatory Agents, Non-Steroidal/*toxicity
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Disease Models, Animal
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Gastric Mucosa/*drug effects/enzymology/pathology
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Glucosamine/metabolism
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Indomethacin/*toxicity
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Intestine, Small/*drug effects/pathology
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Male
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Peroxidase/metabolism
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Rats
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Rats, Sprague-Dawley
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Time Factors
5.Difficult Establishment of a Chronic Nonsteroidal Anti-inflammatory Drugs Induced Gastric Inflammation Rat Model due to Gastric Adaptation and Small Bowel Damage.
Byoung Hwan LEE ; Nayoung KIM ; Ryoung Hee NAM ; Ju Yup LEE ; Hye Seung LEE ; Chang Hee LEE ; Ji Hyun PARK ; Dong Ho LEE
The Korean Journal of Gastroenterology 2014;63(6):341-347
BACKGROUND/AIMS: The prevalence of peptic ulcer disease has not decreased mainly due to an increase in the use of NSAIDs. This study was conducted in order to determine whether a chronic NSAID-induced gastric inflammation model could be established by repeated administration of NSAID. METHODS: Indomethacin (10 mg/kg) was administered once per week for six weeks in 8- and 26-week rats and animals were sacrificed every week after administration. Gross ulcer index, histologic damage index, myeloperoxidase (MPO) activity, and mucus (glucosamine) levels were measured. Small bowel damage was also evaluated. RESULTS: Gross gastric damage index showed a peak level at three weeks and then decreased slowly in the 26-week indomethacin group. Gastric mucosal glucosamine level increased in both the 8-week (p=0.038) and 26-week groups (p=0.007). In addition, gastric mucosal MPO level decreased in the 8-week group (p=0.018) but did not show a decrease in the 26-week group. Small bowel damage began to occur at three weeks during the schedule and eight of 36 rats (22.2%) died due to perforation or peritonitis of the small bowel in the 8- and 26-week indomethacin groups, respectively. CONCLUSIONS: Due to gastric adaptation and small bowel damage, repeated administration of NSAID to experimental animals may not be an adequate method for establishment of the chronic gastric inflammation model.
Animals
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Anti-Inflammatory Agents, Non-Steroidal/*toxicity
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Disease Models, Animal
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Gastric Mucosa/*drug effects/enzymology/pathology
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Glucosamine/metabolism
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Indomethacin/*toxicity
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Intestine, Small/*drug effects/pathology
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Male
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Peroxidase/metabolism
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Rats
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Rats, Sprague-Dawley
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Time Factors
6.Pomegranate leaf attenuates lipid absorption in the small intestine in hyperlipidemic mice by inhibiting lipase activity.
Xuan YU ; Xin-Pei WANG ; Fan LEI ; Jing-Fei JIANG ; Jun LI ; Dong-Ming XING ; Li-Jun DU
Chinese Journal of Natural Medicines (English Ed.) 2017;15(10):732-739
Pomegranate leaf (PGL) has a definite role in regulating lipid metabolism. However, pharmacokinetic results show the main active ingredient, ellagic acid, in PGL has lower oral bioavailability, suggesting that the lipid-lowering effect of PGL may act through inhibiting lipid absorption in the small intestine. Our results demonstrated that pomegranate leaf and its main active ingredients (i.e., ellagic acid, gallic acid, pyrogallic acid and tannic acid) were capable of inhibiting pancreatic lipase activity in vitro. In computational molecular docking, the four ingredients had good affinity for pancreatic lipase. Acute lipid overload experiments showed that a large dosage of PGL significantly reduced serum total cholesterol (TG) and triglycerides (TC) levels in addition to inhibiting intestinal lipase activity, which demonstrated that PGL could inhibit lipase activity and reduce the absorption of lipids. We also found that PGL could reverse the reduced tight-junction protein expression due to intestinal lipid overload, promote Occludin and Claudin4 expression in the small intestine, and enhance the intestinal mucosal barrier. In conclusion, we demonstrated that PGL can inhibit lipid absorption and reduce blood TG and TC by targeting pancreatic lipase, promoting tight-junction protein expression and thereby preventing intestinal mucosa damage from an overload of lipids in the intestine.
Animals
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Enzyme Inhibitors
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administration & dosage
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chemistry
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Humans
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Hyperlipidemias
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drug therapy
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enzymology
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metabolism
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Intestinal Absorption
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Intestine, Small
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metabolism
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Kinetics
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Lipase
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chemistry
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metabolism
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Lipid Metabolism
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Lythraceae
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chemistry
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Male
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Mice
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Mice, Inbred ICR
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Plant Extracts
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administration & dosage
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chemistry
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Plant Leaves
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chemistry
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Triglycerides
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metabolism
7.Sodium tanshinone II A sulfonate ameliorates microcirculatory disturbance of small intestine by attenuating the production of reactie oxygen species in rats with sepsis.
Wei ZHU ; Qing LU ; Lei WAN ; Jun FENG ; Hua-Wen CHEN
Chinese journal of integrative medicine 2016;22(10):745-751
OBJECTIVETo examine whether sodium tanshinone II A sulfonate (STS), the main effective component of Salvia miltiorrhiza is effective in relieving the microcirculatory disturbance of small intestine by suppressing the production of reactive oxygen species (ROS) in rats with sepsis.
METHODSA rat model of sepsis was induced by cecal ligation and puncture (CLP). Rats (n =40) were randomly divided into 4 groups: sham-operated group (sham, n =10), sepsis group (CLP, n =10), STS treatment group (STS, n =10) and ROS scavenger dimethylthiourea (DMTU, n =10) group. Animals in the STS group were injected with STS (1 mg/kg) for 10 min through the right external jugular vein after the CLP operation, and animals in the CLP group were given the same volume of normal saline after the CLP operation. Animals in the DMTU group were intraperitoneally injected with 5 mL/kg of 20% DMTU 1 h before CLP. The histopathologic changes in the intestinal tissues and changes of mesenteric microcirculation were observed. The levels of ROS in intestinal tissues from each group were qualitatively evaluated using a fluorescent microscope. The expressions of apoptosis signal-regulating kinase (ASK1), phosphorylated ASK1 (phospho-ASK1), p38 mitogen-activated protein kinases (p38 MAPK), phosphorylated p38 MAPK (phospho-p38 MAPK) and tissue factor (TF) were determined by Western blotting.
RESULTSIt was shown that there were obvious microcirculatory disturbance (P <0.05) and tissue injuries in intestinal tissues after CLP operation. The levels of ROS production, phospho-ASK1, phospho-p38 MAPK and TF were increased. Both STS and DMTU suppressed ROS, phospho-ASK1, phospho-p38 MAPK and TF production, and ameliorated the microcirculatory disturbance and tissues injury (P <0.01).
CONCLUSIONSTS can ameliorate the microcirculatory disturbance of the small intestine by attenuating the production of ROS in rats with sepsis.
Animals ; Intestine, Small ; blood supply ; drug effects ; pathology ; MAP Kinase Kinase Kinase 5 ; metabolism ; Male ; Microcirculation ; drug effects ; Phenanthrenes ; chemistry ; pharmacology ; therapeutic use ; Phosphorylation ; drug effects ; Rats, Wistar ; Reactive Oxygen Species ; metabolism ; Sepsis ; drug therapy ; enzymology ; pathology ; physiopathology ; Thromboplastin ; metabolism ; p38 Mitogen-Activated Protein Kinases ; metabolism