• The Korean Journal of Physiology and Pharmacology
• /
• 제3권3호
• /
• pp.263-273
• /
• 1999

The role of phospholipase $A_2\;(PLA_2)$ in acute lung leak induced by intestinal ischemia was investigated in association with neutrophilic respiratory burst. To induce lung leak, we generated intestinal ischemia for 60 min prior to the 120 min reperfusion by clamping superior mesenteric artery in Sprague-Dawley rats. Acute lung leak was confirmed by the increased lung leak index and protein content in bronchoalveolar fluid. These changes were inhibited by mepacrine, the non-specific $PLA_2$ inhibitor. The lung myeloperoxidase (MPO) activity denoting the pulmonary recruitment of neutrophils was increased by intestinal I/R, but decreased by mepacrine. Simultaneously, the number of leukocytes in bronchoalveolar fluid was increased by intestinal ischemia/reperfusion (I/R) and decreased by mepacrine. Gamma glutamyl transferase activity, an index of oxidative stress in the lung, was increased after intestinal I/R but decreased by mepacrine, which implicates that $PLA_2$ increases oxidative stress caused by intestinal I/R. The $PLA_2$ activity was increased after intestinal I/R not only in the intestine but also in the lung. These changes were diminished by mepacrine. In the cytochemical electron microscopy to detect hydrogen peroxide, intestinal I/R increased the generation of the hydrogen peroxide in the lung as well as in the intestine. Expression of interleukin-1 (IL-1) in the lung was investigated through RT-PCR. The expression of IL-1 after intestinal I/R was enhanced, and again, the inhibition of $PLA_2$ suppressed the expression of IL-1 in the lung. Taken together, intestinal I/R seems to induce acute lung leak through the activation of $PLA_2$, the increase of IL-1 expression associated with increased oxidative stress by neutrophilic respiratory burst.

• The Korean Journal of Physiology
• /
• 제1권1호
• /
• pp.51-56
• /
• 1967

In order to find out the effects of GABA on the rabbit's intestinal motility, the following experiments were carried out using Magnus method and the results obtained were as follows: 1. GABA inhibited the intestinal motility of rabbits initially. 2. GABA potentiated the inhibitory action of adrenaline and nor-adrenaline. 3. GABA inhibited the accelerating activity of acetylcholine on the intestinal motility by its anti acetylcholine effect. 4. The inhibitory action of GABA was unaffected with atropinization, strychnin, picrotoxin treatment, but the accelerating activity of GABA observed in some cases was only in the picrotoxin treatment.

• 대한의생명과학회지
• /
• 제18권3호
• /
• pp.218-226
• /
• 2012

Dopamine is an enteric neurotransmitter that regulates gastrointestinal motility. This study was done to investigate whether dopamine modulates spontaneous pacemaker activity in cultured interstitial cells of Cajal (ICCs) from mouse using whole cell patch clamp technique, RT-PCR and live $Ca^{2+}$ imaging analysis. ICCs generate pacemaker inward currents at a holding potential of -70 mV and generate pacemaker potentials in current-clamp mode. Dopamine did not change the frequency and amplitude of pacemaker activity in small intestinal ICCs. On the contrary dopamine reduced the frequency and amplitude of pacemaker activity in large intestinal ICCs. RT-PCR analysis revealed that Dopamine2 and 4-receptors are expressed in c-Kit positive ICCs. Dopamine2 and 4 receptor agonists inhibited pacemaker activity in large intestinal ICCs mimicked those of dopamine. Domperidone, dopamine2 receptor antagonist, increased the frequency of pacemaker activity of large intestinal ICCs. In $Ca^{2+}$-imaging, dopamine inhibited spontaneous intracellular $Ca^{2+}$ oscillations of ICCs. These results suggest that dopamine can regulate gastrointestinal motility through modulating pacemaker activity of large intestinal ICCs and dopamine effects on ICCs are mediated by dopamine2 receptor and intracellular $Ca^{2+}$ modulation.

• 농업과학연구
• /
• 제48권3호
• /
• pp.447-454
• /
• 2021

This study was conducted to evaluate the effects of different copper sources (inorganic and organic) on the growth performance, fecal copper excretion, intestinal morphology, and health in growing pigs. A total of 40 growing pigs (30.22 ± 1.92 kg) were randomly assigned to 5 dietary treatments: a basal control diet (CON), 4 experimental diets supplemented with either copper sulfate (CuSO₄), Cu-glycine complex (CuGly), Cu-amino acid complex (CuAA), or Cu-hydroxy-4-methylthio butanoate chelate complex (CuHMB) at 100 ppm, respectively. At the end of the study (28 days), fecal and blood samples were collected, and the pigs were slaughtered to determine the intestinal morphology. During the 28 days of the experimental period, pigs fed the inorganic and organic copper showed a higher average daily gain (p < 0.01) and gain feed ratio (p < 0.01). There were no differences in mineral concentrations of the serum; however, the copper concentration of the feces was lower (p < 0.01) in the CuAA and CuHMB groups. The intestinal morphology and blood profiles did not significantly differ between the groups. In conclusion, the organic copper sources (CuAA and CuHMB) can be used as a growth promoter to replace the CuSO₄ without any negative effects on health in growing pigs and to reduce fecal copper excretion.

• The Korean Journal of Physiology and Pharmacology
• /
• 제14권3호
• /
• pp.151-156
• /
• 2010

This study was performed to investigate the role of glutamate neurotransmitter system on gastrointestinal motility in a middle cerebral artery occlusion (MCAO) model of rats. The right middle cerebral artery was occluded by surgical operation, and intestinal transit and geometric center as a parameter of gastrointestinal motility and expression of c-Fos protein in the insular cortex and cingulate cortex were measured at 2 and 12 h after MCAO. Intestinal transit was $66.3{\pm}7.5%$ and $62.3{\pm}5.7%$ 2 and 12 h after sham operation, respectively, and MCAO significantly decreased intestinal transit to $39.0{\pm}3.5%$ and $47.0{\pm}5.1%$ at 2 and 12 h after the occlusion, respectively (p<0.01). The geometric center was $5.6{\pm}0.4$ and $5.2{\pm}0.9$ at 2 and 12 h after sham operation, respectively, and MCAO significantly decreased geometric center to $2.9{\pm}0.8$ and $3.0{\pm}0.3$ at 2 and 12 h after the occlusion, respectively (p<0.01). In control animals, injection of atropine decreased intestinal transit to $35.9{\pm}5.2%$, and injection of glutamate NMDA receptor antagonist, MK-801, decreased intestinal transit to $28.8{\pm}9.5%$. Pretreatment with MK-801, a glutamate NMDA receptor antagonist, in the MCAO group decreased intestinal transit to $11.8{\pm}3.2%$, which was significantly decreased compared to MCAO group (p<0.01). MCAO markedly increased the expression of c-Fos protein in the insular cortex and cingulate cortex ipsilateral to the occlusion 2 h after MCAO, and pretreatment with MK-801 produced marked reduction of c-Fos protein expression compared to MCAO group (p<0.01). These results suggest that modulation of gastrointestinal motility after MCAO might be partially mediated through a glutamate NMDA receptor system.

• The Korean Journal of Physiology
• /
• 제16권2호
• /
• pp.159-163
• /
• 1982

Vasoactive intestinal peptide (VIP) found in duodenal mucosa originally has been suggested as a neurotransmitter. Its localization, however, now known, is not limited to the gastrointestinal tract, but scattered at many different kinds of tissues, smooth muscles, endocrine gland and exocrine gland as well as central and peripheral neural tissues. To investigate the effect of VIP on renal function, an experiment has been done in anesthetized male rats. The results obtained were: 1) Urinary output and creatinine clearance decreased significantly during the period of infusion of VIP, 2.0ug/rat/7minutes. 2) Urinary excretion of sodium, potassium and chloride decreased but without significance by infusion of VIP. 3) Blood pressure, systolic and diastolic, decreased by VIP administered intravenously in the period of infusion. 4) Changes of urinary output, sodium and chloride excretion was correlated with changes of creatinine clearance. The above data suggest that VIP administered intravenously can suppress the renal hemodynamics indirectly, and also decrease electrolyte excretion through its renal hemodynamic change.

• The Korean Journal of Physiology and Pharmacology
• /
• 제3권4호
• /
• pp.405-414
• /
• 1999

The role of platelet-activating factor (PAF) was investigated in intestinal ischemia/reperfusion (I/R) induced acute lung injury associated with oxidative stress. To induce acute lung injury following intestinal I/R, superior mesenteric arteries were clamped with bulldog clamp for 60 min prior to the 120 min reperfusion in Sprague-Dawley rats. Acute lung injury by intestinal I/R was confirmed by the measurement of lung leak index and protein content in bronchoalveolar lavage (BAL) fluid. Lung leak and protein content in BAL fluid were increased after intestinal I/R, but decreased by WEB 2086, the PAF receptor antagonist. Furthermore, the pulmonary accumulation of neutrophils was evaluated by the measurement of lung myeloperoxidase (MPO) activity and the number of neutrophils in the BAL fluid. Lung MPO activity and the number of neutrophils were increased (p＜0.001) by intestinal I/R and decreased by WEB 2086 significantly. To confirm the oxidative stress induced by neutrophilic respiratory burst, gamma glutamyl transferase (GGT) activity was measured. Lung GGT activity was significantly elevated after intestinal I/R (p<0.001) but decreased to the control level by WEB 2086. On the basis of these experimental results, phospholipase $A_2\;(PLA_2),$ lysoPAF acetyltransferase activity and PAF contents were measured to verify whether PAF is the causative humoral factor to cause neutrophilic chemotaxis and oxidative stress in the lung following intestinal I/R. Intestinal I/R greatly elevated $PLA_2$ activity in the lung as well as intestine (p<0.001), whereas WEB 2086 decreased $PLA_2$ activity significantly (p<0.001) in both organs. LysoPAF acetyltransferase activity, the PAF remodelling enzyme, in the lung and intestine was increased significantly (p<0.05) also by intestinal I/R. Accordingly, the productions of PAF in the lung and intestine were increased (p<0.001) after intestinal I/R compared with sham rats. The level of PAF in plasma was also increased (p<0.05) following intestinal I/R. In cytochemical electron microscopy, the generation of hydrogen peroxide was increased after intestinal I/R in the lung and intestine, but decreased by treatment of WEB 2086 in the lung as well as intestine. Collectively, these experimental results indicate that PAF is the humoral mediator to cause acute inflammatory lung injury induced by intestinal I/R.

• Journal of Ginseng Research
• /
• 제47권2호
• /
• pp.265-273
• /
• 2023

Background: The intestinal microbiota is an important regulator of bone health. In previous studies we have shown that intestinal microbiota dysbiosis, induced by treatment with broad spectrum antibiotics (ABX) followed by natural repopulation, results in gut barrier dysfunction and bone loss. We have also shown that treatment with probiotics or a gut barrier enhancer can inhibit dysbiosis-induced bone loss. The overall goal of this project was to test the effect of Korean Red Ginseng (KRG) extract on bone and gut health using antibiotics (ABX) dysbiosis-induced bone loss model in mice. Methods: Adult male mice (Balb/C, 12-week old) were administered broad spectrum antibiotics (ampicillin and neomycin) for 2 weeks followed by 4 weeks of natural repopulation. During this 4-week period, mice were treated with vehicle (water) or KRG extract. Other controls included mice that did not receive either antibiotics or KRG extract and mice that received only KRG extract. At the end of the experiments, we assessed various parameters to assess bone, microbiota and in vivo intestinal permeability. Results: Consistent with our previous results, post-ABX- dysbiosis led to significant bone loss. Importantly, this was associated with a decrease in gut microbiota alpha diversity and an increase in intestinal permeability. All these effects including bone loss were prevented by KRG extract treatment. Furthermore, our studies identified multiple genera including Lactobacillus and rc4-4 as well as Alistipes finegoldii to be potentially linked to the effect of KRG extract on gut-bone axis. Conclusion: Together, our results demonstrate that KRG extract regulates the gut-bone axis and is effective at preventing dysbiosis-induced bone loss in mice.

• 한국초지조사료학회지
• /
• 제38권2호
• /
• pp.74-83
• /
• 2018

The objectives of this study was to evaluate the degradability and digestibility of crude protein (CP), rumen undegradable protein (RUP), and individual amino acids (AA) on six by-product feedstuffs (BPF) (rice bran, RB; wheat bran, WB; corn gluten feed, CGF; tofu residue, TR; spent mushroom substrate from Pleurotus ostreatus, SMSP; brewers grain, BG) as ruminants feed. Three Hanwoo steers (40 months old, $520{\pm}20.20kg$ of body weight) fitted with a permanent rumen cannula and T-shaped duodenal cannula were used to examine of the BPF using in situ nylon bag and mobile bag technique. The bran CGF (19.2%) and food-processing residue BG (19.7%) had the highest CP contents than other feeds. The RUP value of bran RB (39.7%) and food-processing residues SMSP (81.1%) were higher than other feeds. The intestinal digestion of CP was higher in bran RB (44.2%) and food-processing residues BG (40.5%) than other feeds. In addition, intestinal digestion of Met was higher in bran RB (55.7%) and food-processing residues BG (44.0%) than other feeds. Overall, these results suggest that RB and BG might be useful as main raw ingredients in feed for ruminants. Our results can be used as baseline data for ruminant ration formulation.

• 고려인삼학회:학술대회논문집
• /
• 고려인삼학회 2007년도 춘계 학술대회
• /
• pp.18-18
• /
• 2007