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Biomedical subjects

S Oh-ishi

Publications and source records attributed to S Oh-ishi.

At least 37 records · Page 2Linked to original sources
PubMed1997

Concordant induction of prostaglandin E2 synthase with cyclooxygenase-2 leads to preferred production of prostaglandin E2 over thromboxane and prostaglandin D2 in lipopolysaccharide-stimulated rat peritoneal macrophages.

Rat peritoneal macrophages were stimulated with lipopolysaccaride (LPS) for various periods and their ability to convert exogenous arachidonic acid to various prostanoids was examined. Unstimulated cells, which expressed cyclooxygenase (COX)-1 but not COX-2, produced thromboxane (TX) B2 > prostaglandin (PG) D2 > PGE2, whereas cells stimulated for 6-12 h with LPS exhibited marked increase in conversion to PGE2, which paralleled COX-2 induction, with minimal change in conversion to TXB2 and PGD2. Pharmacological studies showed that formation of PGE2 was mediated predominantly by COX-2, PGD2 by COX-1, and TXB2 by both COX-1 and COX-2 depending upon the timing of LPS stimulation. Measurement of the conversion of exogenous PGH2 to each prostanoid in cell lysates demonstrated LPS-dependent increase in PGE2 synthase activity that was degenerated by pretreatment with actinomycin D or cycloheximide. Thus, concordant induction of terminal PGE2 synthase with COX-2 leads to the preferred production of PGE2 to TXB2 and PGD2 by LPS-stimulated macrophages.

Animals↗
PubMed1997

Effects of endurance training on superoxide dismutase activity, content and mRNA expression in rat muscle.

1. The purpose of the present study was to investigate the changes in superoxide dismutase (SOD) isoenzyme (Mn(2+)-SOD and Cu2+, Zn(2+)-SOD) activities, contents and mRNA expressions in rat skeletal muscle during endurance training and a single bout of exercise. 2. Thirty-eight male Wistar rats were divided into untrained (U) and trained (T) groups. The T group rats were treadmill-trained for 9 weeks. The activity, content and mRNA expression of Mn(2+)-SOD and Cu2+, Zn(2+)-SOD were determined in the soleus muscle of each rat. 3. Mn(2+)-SOD activity and content in the T group were significantly higher than in the U group, both at rest (22 and 21%, respectively) and after exercise (24 and 46%, respectively), while a single bout of exercise affected neither the activity nor content of Mn(2+)-SOD in either group. 4. The content of Cu2+,Zn(2+)-SOD in both groups was not different at rest and after exercise, although its activity at rest was significantly higher in the T group than in the U group (by 29%). 5. After exercise, the expression of Mn(2+)-SOD mRNA was markedly attenuated only in the U group (49%); the expression of Cu2+,Zn(2+)-SOD mRNA was not influenced by exercise. 6. Our results suggest that adequate endurance training increases both the activity and content of Mn(2+)-SOD and that untrained rats are rather susceptible to oxidative stress during physical exercise. It thus appears that Mn(2+)-SOD provides a reliable index of physical training. 7. The results obtained in the present study also suggest that muscle has the capacity of responding to training in such a manner as to reduce the potential harm arising from the accumulation of oxygen free radicals resulting from enhanced metabolic activity.

Animals↗
PubMed1997

Endurance training improves the resistance of rat diaphragm to exercise-induced oxidative stress.

The current study was designed to test the hypothesis that endurance training improves the ability of the diaphragm muscle to resist exercise-induced oxidative stress. Twenty-eight male Wistar rats were assigned to either untrained or trained groups. Trained rats were treadmill-trained for 9 wk. Each group was subdivided into acutely exercised or nonexercised groups. Diaphragm muscle from each rat was analyzed to determine the levels of certain antioxidant enzymes: Mn-superoxide dismutase (Mn-SOD), Cu,Zn-superoxide dismutase (Cu,Zn-SOD), glutathione peroxidase, and catalase. In addition, interleukin-1 and myeloperoxidase levels were determined. Endurance training upregulated all of the antioxidant enzymes. Conversely, acute exercise increased glutathione peroxidase and catalase in untrained rats, while it had no overt effect on any antioxidant enzymes in trained rats. Both Mn-SOD and Cu,Zn-SOD contents and activities were increased with endurance training. However, the mRNA expressions of both forms of SOD did not show any significant change with endurance training. Acute exercise also increased the levels of interleukin-1 and myeloperoxidase in untrained rats but not in trained rats. Moreover, acute exercise significantly increased the ability of neutrophils to produce superoxide, especially in untrained rats. The results from this study demonstrate that endurance training can upregulate certain antioxidant enzyme activities in rat diaphragm muscle, indicating the potential for improvement of the resistance to intracellular reactive oxygen species. The results of this study also suggest that acute exercise may cause oxidative damage in rat diaphragm through the activation of the inflammatory pathway and that endurance training may minimize such an extracellular oxidative stress by acute exercise.

Animals↗
PubMed1997

[Analysis of chemical mediators involved in acute inflammatory reaction with the rat pleurisy model].

Mediators involved in acute inflammation were explored by using rat pleurisies induced by carrageenin or zymosan. The kallikrien-kinin system and eicosanoids were the main mediators responsible for plasma exudation in carrageenin-induced rat pleurisy, while histamine, PAF and the complement system could be the main mediators involved in the vascular permeability increase to cause plasma exudation into the pleural cavity in zymosan-induced rat pleurisy. Several chemokines were detected in the pleural exudates of carrageenin-pleurisy as well as those of zymosan-pleurisy; and exogenous recombinant TNF alpha, IL-1, IL-6 and CINC induced neutrophil migration into rat pleural cavity. These results suggest that these chemokines, directly or indirectly, may partly cause neutrophil migration in the pleural exudates during carrageenin- and zymosan-induced pleurisy. In addition, chemokine production in response to prostanoids and PAF production in response to arachidonic acid were also suggested.

Animals↗
PubMed1997

[Induction of bradykinin B1 receptor in rats].

We found the time-dependent induction of the systemic hypotensive response to des-Arg9-bradykinin and the contractile response of ileum of rats to des-Arg9-bradykinin. Both induced responses to des-Arg9-bradykinin were inhibited by treatment with a B1 receptor competitive antagonist, while the responses to bradykinin was constant throughout the experiment and was not influenced by the B1 antagonist, suggesting that these responses occur via a B1 receptor. The potencies of des-Arg9-bradykinin in these responses were comparable to those of bradykinin at a molar base. The other characteristics of this phenomenon is that several hours were required to the induction of these responses. In a case of hypotensive response, intravenous LPS pretreatment was necessary, but not for the induction of contraction in ileum preparation. Treatment with actinomycin D or cycloheximide throughout the experiment suppressed the induction of the contractile response to des-Arg9-bradykinin. The expression of B1 receptor gene was also confirmed by a RT-PCR method. Therefore, we concluded that these responses to des-Arg9-bradykinin occurred via a B1 receptor, which could be newly generated time-dependently.

Animals↗
PubMed1997

Effects of swimming training on brown-adipose-tissue activity in obese ob/ob mice: GDP binding and UCP m-RNA expression.

Brown adipose tissue (BAT) of obese animals is generally in a relatively atrophied and thermogenically quiescent state. The aim of the current study was to investigate the effect of swimming training on BAT activity in lean and obese (ob/ob) mice. The trained mice underwent a 6-week endurance swimming training (1 h/day, 5 days/week) in water at 35-36 degrees C. The swimming training significantly increased BAT mass and its protein content in both the lean and obese mice, suggesting hypertrophy. After swimming training, the amounts of protein and guanosine 5'-diphosphate binding in the mitochondria recovered from BAT of both mice increased significantly as compared with the respective sedentary groups, whereas the uncoupling protein (UCP) content increased significantly only in lean mice. After swimming training, the level of UCP mRNA expression did not change substantially in lean mice but appeared to increase in obese mice. The results obtained here suggest that swimming training leads to an increase in the nonshivering thermogenesis of obese mice in addition to lean mice.

Adipose Tissue, Brown↗
PubMed1997

Effect of swimming training on antioxidant enzymes in kidney of young and old mice.

The current study was undertaken to investigate the effect of swimming training on the antioxidant enzyme system in kidney of young and old mice. Both young and old mice, aged 2 and 26 months old, respectively, were divided into the sedentary and swimming-trained groups. The trained mice underwent a 6-week swimming program (1 h/day, 5 days/week) in water at 35-36 degrees C. Cu,Zn-superoxide dismutase (Cu,Zn-SOD) activity was significantly decreased with aging but was not influenced by swimming training, such changes being similar to those noted for catalase activity rather than for glutathione peroxidase activity. After swimming training Mn-SOD activity increased significantly only in old mice but was unaffected by aging. Although neither aging nor swimming training had overt effect on the expression of Cu,Zn-SOD mRNA, the immunoreactive Cu,Zn-SOD content in young mice decreased significantly after the training. Meanwhile, Mn-SOD mRNA expression in old mice was reduced by half after swimming training, accompanied by a significant decrease in its immunoreactive content; unexpectedly, however, Mn-SOD content in young mice did not parallel its mRNA expression. These findings suggest that the antioxidant enzyme system in mouse kidney trends to be down-regulated with aging, and that swimming training fails to attenuate such reduced levels of the antioxidant enzymes.

Aging↗
PubMed1996

Swimming training improves brown-adipose-tissue activity in young and old mice.

The impairment of brown adipose tissue (BAT) thermogenic activity with aging has been well documented. The current study investigated the effect of swimming training on BAT activity in 2-month-old (young) and 26-month-old (old) male mice. The trained mice underwent a 6-week swimming program (1 h/day, 5 days/week) in water at 35-36 degrees C. Compared with young sedentary mice, the BAT-to-body mass ratio was markedly smaller in old sedentary mice, accompanied by the decreased amount of protein, whereas there was no significant difference in uncoupling protein (UCP) content, UCP mRNA expression, or guanosine 5'-diphosphate (GDP) binding (an index of UCP activity) between young and old mice. Meanwhile, the swimming training definitely increased BAT mass and its protein content in both the young and old mice, suggesting hypertrophy and hyperplasia. In addition, after the swimming training, the amounts of protein, UCP antigen, and GDP binding in the mitochondria recovered from BAT of both mice increased significantly as compared with the respective sedentary groups, while the expression of UCP mRNA did not vary substantially. These findings suggest that, irrespective of age, swimming training enhances the thermogenic activity and capacity in BAT of mice.

Adipose Tissue, Brown↗
PubMed1996

Inhibitory effect of arachidonic acid on platelet-activating factor production in rat neutrophils.

Platelet-activating factor production in rat neutrophils in response to opsonized zymosan was suppressed dose dependently in the presence of 10-100 microM arachidonic acid. The amount of lyso-PAF was also reduced by these doses of arachidonic acid. Phospholipase A2 activity was not changed by addition of arachidonic acid up to 100 microM, but acetyltransferase activity was slightly reduced at a 100 microM concentration of arachidonic acid. Pretreatment with indomethacin did not alter the inhibitory effect of arachidonic acid on PAF production, indicating no involvement of cyclooxgenase products. Triacsin C, an acyl-CoA synthetase inhibitor, reversed the arachidonic acid-induced suppression of lyso-PAF and PAF production, suggesting that arachidonic acid might exert its inhibition via the acylation pathway of lyso-PAF to reduce the availability of lyso-PAF.

Acetyl-CoA C-Acetyltransferase↗
PubMed1996

Effects of prostaglandins and cyclic AMP on cytokine production in rat leukocytes.

Prostaglandins E1, prostaglandin E2, 3-oxa-methano-prostaglandin I1 (SM-10906), a stable prostaglandin I2 analog, and dibutyryl cyclic AMP suppressed the production of tumor necrosis factor and interleukin-1 in lipopolysaccharide-stimulated rat pleural resident monocytic cells, whereas they enhanced the production of interleukin-6 and cytokine-induced neutrophil chemoattractant (CINC), a rat interleukin-8-like chemokine, in these cells. SM-10906 also inhibited the in vivo production of tumor necrosis factor and interleukin-1 in pleural exudates, when injected into the rat pleural cavity concomitantly with carrageenin. The cyclic AMP (cAMP) level in the lipopolysaccharide-stimulated resident cells was increased when the cells were incubated in the presence of prostaglandin E1, prostaglandin E2 or SM-10906. Prostaglandin I2 showed only slight effects. The addition of pentoxifylline, a phosphodiesterase inhibitor, to the incubation mixture increased the cAMP level and also enhanced the effect of prostaglandins, indicating that these regulating actions of prostaglandins may be exerted partly through a mechanism involving an increased intracellular cAMP level.

Alprostadil↗
PubMed1996

Effects of aging and/or training on antioxidant enzyme system in diaphragm of mice.

We investigated the effects of aging and/or swimming training on the antioxidant enzyme system in diaphragm of mice. Young (2 months old) and old (26 months old) male mice were swimming-trained for 6 weeks (1 h/day, 5 days/week). Cu,Zn-Superoxide dismutase (Cu,Zn-SOD) activity was significantly upregulated with aging, and swimming training definitely enhanced the activity only in young mice. Neither aging nor swimming training had overt effect on Mn-SOD activity. Glutathione peroxidase activity in young mice was significantly increased after training, but not in old mice. Both of immunoreactive Cu,Zn-SOD and Mn-SOD were significantly increased with aging but were unaffected by swimming training. Consequently, physical training significantly enhanced the specific activity of Cu,Zn-SOD in young mice, but not in old mice. Meanwhile, swimming training significantly increased xanthine oxidase activity in both age groups, the extent of the increase being greater in old mice than in young mice. We concluded that the antioxidant enzyme system in mouse diaphragm trends to be upregulated with aging, but that swimming training improved the system only in young mouse diaphragm.

Aging↗
PubMed1996

Induction of a B1-receptor mediating hypotensive response in young brown Norway rats.

A hypotensive response to intravenously injected des-Arg9-bradykinin was elicited in young male Brown Norway rats (8-12 weeks-old), when the rats were intravenously injected with endotoxin (30 micrograms/kg) 24 h before they were repeatedly injected with bradykinin or des-Arg9-bradykinin. The potency of this inducible dose-dependent hypotensive response to des-Arg9-bradykinin was comparable to that induced by bradykinin on a molar base (3-30 nmol/kg). A hypotensive response to des-Arg9-bradykinin could also be induced when the rats were pretreated with endotoxin 6 h before. However, the potency of the response was less than that induced by 24-h pretreatment. This inducible response to des-Arg9-bradykinin did not occur in old rats (8-10 months old). Intravenous infusion of a B1-receptor antagonist, des-Arg9-[Leu8]-bradykinin, suppressed the hypotensive response of des-Arg9-bradykinin. These results suggest that the B1-receptor, mediating hypotension in rats, was inducible through time-dependent and age-dependent sensitization by endotoxin pretreatment.

Age Factors↗
PubMed1996

Acute cold stress induces suppressor macrophages in mice.

To elucidate mechanisms underlying acute cold stress-induced immunosuppression, functions of murine peritoneal cells of monocyte/ macrophage lineage from acute cold-stressed mice (exposed to 5 degrees C for 24 h) were investigated. Proliferative responses of spleen cells from control mice (reared at 25 degrees C) stimulated with concanavalin A (ConA) were significantly suppressed by adding peritoneal exudate cells from mice immediately after acute cold stress. The proportion of adherent cells was markedly increased in the peritoneal exudate cells from acute cold-stressed mice. These adherent cells from acute cold-stressed mice were shown to be the cells responsible for the suppressor activity for ConA responses of control spleen cells. Nonadherent cells did not suppress the ConA responses. The adherent cells in peritoneal exudate cells from control mice also suppressed the ConA responses, the inhibitory effect being considerably lower than that from acute cold-stressed mice. Addition of a nitric oxide synthase substrate analogue, NG-monomethyl-L-arginine, to the mixed cell cultures of normal spleen cells and adherent cells from acute cold-stressed mice inhibited nitric oxide release and completely abolished the suppressive effect of the adherent cells, suggesting that reactive nitrogen oxide released from the activated macrophages is apparently involved in the downregulation of proliferative responses of T cells. Thus the present findings suggest that acute cold stress induces macrophages with suppressor function and that this may contribute to the immune-suppressive state seen in spleen cells from acute cold-stressed mice.

Acute Disease↗
PubMed1996

Glucocorticoid-mediated generation of suppressor macrophages with high density Fc gamma RII during acute cold stress.

Acute cold stress induces adherent cells with suppressor function, resulting in immunosuppression. Glucocorticoids (GC) are known as an inhibitor of the immune system and are increased by stress through stimulation of the hypothalamic-pituitary-adrenal axis. To elucidate the mechanisms underlying acute cold stress-induced immunosuppression, functions and surface phenotypes of murine peritoneal cells of the monocyte/macrophage lineage from acute cold-stressed mice (5 C for 3 or 24 h) in addition to the role of GC in the immunomodulation were investigated. Flow cytometric analysis revealed that the proportion of MAC-1+ cells with a high density of Fc gamma RII (Fc gamma RIIbright cells) was markedly increased in the peritoneal exudate cells from acute cold-stressed mice. These Fc gamma RIIbright cells were also stained with F4/80, a monoclonal antibody directed specifically against the mouse mature macrophages. The prominent suppressor activity for Concanavalin A (Con A) responses of control spleen cells was found in Fc gamma RIIbright cells, whereas MAC-1+ cells, with a low density of Fc gamma RII (Fc gamma RIIdull cells), from the stressed mice did not suppress the Con A responses. Fc gamma RIIbright cells from control mice also suppressed the Con A responses; the inhibitory effect was considerably less than that of cells from acute cold-stressed mice. As was anticipated, serum corticosterone levels were markedly increased in acute cold-stressed mice. In addition, expression of GC receptor messenger RNA was observed in Fc gamma RIIbright cells from these mice. The increase in Fc gamma RIIbright cells in peritoneal exudate cells caused by acute cold stress was inhibited by adrenalectomy or administration of a saturating amount of the GC antagonist RU 38486 (mifepristone). On the contrary, administration of the GC agonist, dexamethasone, markedly increased the proportion of Fc gamma RIIbright cells in peritoneal exudate cells of control mice. These results suggest that the generation of Fc gamma RIIbright suppressor cells of monocyte/macrophage lineage by acute cold stress was mediated to a greater or lesser degree by the action of GC through the GC receptor.

Acute Disease↗
PubMed1996

The mediators involved in endotoxin-induced vascular permeability increase in the rat skin and their interactions.

The injection of lipopolysaccharide (LPS) from E. Coli into the dorsal skin of rats caused a dose-dependent increase in vascular permeability as measured by the extravasation over a 40-min period of intravenously injected dye. This increase caused by LPS was attenuated by pretreatment with the bradykinin (BK) receptor antagonist HOE140, the selective platelet-activating factor (PAF) antagonist TCV309, and by combined treatment with mepyramine and methysergide. Combined treatment with HOE140 and TCV309 resulted in further suppression than that achieved with a single treatment alone. By the simultaneous pretreatment with all antagonists, the response was almost totally abolished. On the other hand, indomethacin also inhibited the response induced by LPS, but not those induced by BK and PAF itself. A small dose of BK or histamine synergistically potentiated the effect of PAF when simultaneously injected. These results suggest that BK, PAF, histamine/serotonin and prostaglandins are involved in the LPS-induced increase in vascular permeability, where PAF, in addition to its direct action, potentiates the response to BK and histamine, and prostaglandins potentiate the actions of other mediators without its direct action.

Animals↗
PubMed1996

Decreased vascular sensitivity after acute exercise and chronic exercise training in rat thoracic aorta.

The effects of acute and chronic physical exercise on the sensitivity of isolated aorta to norepinephrine were investigated. After chronic exercise, the EC50 values for norepinephrine increased 3.1-fold and 2.3-fold in endothelium-intact and in endothelium-denuded aorta, respectively. The attenuated sensitivity of aorta to norepinephrine after chronic exercise was still evident in endothelium-denuded aorta, but to a lesser extent than in endothelium-intact aorta. After acute exercise, in control rats, the EC50 values increased 7.8-fold and 5.4-fold in endothelium-intact and endothelium-denuded aorta, respectively. The attenuated sensitivity of aorta to norepinephrine after an acute exercise was still evident in endothelium-denuded aorta. In trained rats, the EC50 values increased 2.3-fold and 2.6-fold in endothelium-intact and endothelium-denuded aorta, respectively. Thus, acute exercise was less effective in trained than in control rats. No significant difference in 60 mM KCl-induced tension between control and trained rats was observed with or without endothelium after acute and chronic exercise. The results suggest that levels of endothelium-dependent releasing factor may increase in response to norepinephrine after acute and chronic exercise. In addition, the attenuated sensitivity of aorta to norepinephrine after acute and chronic exercise may also result from the change(s) in the receptor sites. However, the degree of desensitization caused by acute exercise was less in the rats adapted to chronic exercise than in the sedentary control rats.

Adrenergic alpha-Agonists↗
PubMed1995

Involvement of bradykinin in endotoxin-induced vascular permeability increase in the skin of rats.

The aim of the present study was to investigate the role of bradykinin as well as that of platelet-activating factor in the endotoxin-induced acute vascular permeability increase in the dorsal skin of rats by use of kininogen-deficient and normal Brown-Norway rats. In the kininogen-deficient rats, the dose-dependent dye exudation induced by endotoxin was about one half of that in the normal rats at any doses of endotoxin tested (0.1-1.0 mg per site), whereas the dose-response curves obtained by bradykinin (1-100 nmol per site), platelet-activating factor (0.1-1 nmol per site) or histamine (50-500 nmol per site) were the same in both rats. This effect induced by endotoxin in the kininogen-deficient rats was not changed by pretreatment with a bradykinin B2 receptor antagonist, HOE140 (D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]bradykinin, 1 mg kg-1 i.v.), whereas the endotoxin-induced response in the normal rats was attenuated by the receptor antagonist. These responses in both kininogen-deficient and normal rats were significantly inhibited by a selective platelet-activating factor antagonist, TCV309 (3-bromo-5-[N-phenyl-N-[2-[[2-(1,2,3,4,-tetrahydro-2- isoquinolylcarbonyl-oxy)-ethyl]-carbamoyl]-ethyl]carbamoyl]-1-prop yl- pyridinium nitrate, 0.1 mg kg-1 i.v.). These results suggest that bradykinin could be one of the major mediators in the endotoxin-induced vascular permeability increase in rat skin in addition to platelet-activating factor.

Animals↗