Biomedical subjects

T Hisamitsu

Publications and source records attributed to T Hisamitsu.

81 records · Page 5Linked to original sources

PubMedDate not supplied

Inhibitory effect of electroacupuncture on murine collagen arthritis and its possible mechanisms.

The influence of electroacupuncture (EA), a traditional Chinese medical treatment, on type II collagen-induced arthritis (CIA) was examined in DBA/IJ mice in vivo. Mice were immunized intradermally twice at a 3-week interval with bovine type II collagen (C II). EA stimulation, begun on day 21 simultaneously with the second immunization, was applied at the acupoint equivalent to GV4 three times a week for 3 weeks. The results showed that EA delayed the onset, attenuated the severity of arthritis, and reduced the anti-collagen antibody level. Furthermore, we investigated the impact of EA on the productions of endogenous interleukin-1 beta (IL-1 beta) and prostaglandin E2 (PGE2), and the levels of IL-1 beta mRNA in splenocytes and synovial tissues from C II immunized mice on day 45 and cyclooxygenase-2 (COX-2) mRNA in lipopolysaccharide (LPS)-stimulated macrophages of normal mice by using reverse transcriptase-polymerase chain reaction (RT-PCR). EA stimulation significantly inhibited the concentrations of splenic endogenous IL-1 beta and serum PGE2. The expression of IL-1 beta mRNA in spleen cells was obviously down-regulated and that in synovial tissues was modestly affected by EA. COX-2 mRNA was highly expressed in cultured peritoneal macrophages when stimulated with LPS. Previous treatment with EA also reduced LPS-stimulated induction of COX-2 mRNA. These data suggest that EA has an inhibitory effect on murine CIA, and the partial mechanism of its therapeutic result may be attributed to inhibiting the productions of IL-1 beta and PGE2 by suppressing the IL-beta and COX-2 gene activations.

Animals↗

PubMedDate not supplied

Influence of anti-allergic agents on in vivo expression of co-stimulatory molecules in normal mice.

The co-stimulatory signal provided by the interaction between CD28 and its ligands, CD80 and CD86, is critical for T cell activation. Engagement of CD40 and CD40L is also essential for IgE synthesis and secretion. In the present study, we examined the influence of anti-allergic drugs on co-stimulatory molecule (CD40, CD80 and CD86) expression in normal mouse splenocytes by flow cytometry. Treatment of BALB/c mice with azelastine (AZ) at a dose of 50.0 micrograms/kg/day, which is the most effective therapeutic dose, for two weeks scarcely affected the expression of co-stimulatory molecules CD40, CD80 and CD86 on splenocytes, whereas a three-week treatment strongly suppressed the expression of these molecules. We also examined the influence of terfenadine (TR) on co-stimulatory molecule expression. The expression of molecules on splenocytes was inhibited when donor mice were treated orally with 2.0 mg/kg/day of TR for three weeks. However, it was not inhibited during a two-week period treatment. These results suggest that the attenuating effects of anti-allergic agents on the diseases may be explained, in part, by their inhibitory action of co-stimulatory molecule expression.

Animals↗

PubMedDate not supplied

Suppressive effects of azelastine hydrochloride on CD40 expression in mice.

The present study was designed to examine the influence of an anti-allergic agent, azelastine hydrochloride (AZ) on a co-stimulatory molecule, CD40 expression in actively sensitized mice. BALB/c mice were sensitized by intraperitoneal injection of two doses of dinitrophenylated-ovalbumin and Al(OH)3 at one-week intervals. The mice were treated orally with 0.1 mg/kg of AZ once a day for 14 days starting the same day of booster sensitization. AZ treatment of mice caused the significant suppression of total serum IgE concentration on Day 21 after the first sensitization. However, AZ treatment scarcely affected IL-4 concentration in aqueous spleen extracts. Flowcytometric analysis revealed the suppressive effects of AZ on CD40 expression on sensitized-spleen cells. These data may suggest that AZ suppresses the production of IgE through the inhibition of CD40 expression.

Animals↗

PubMedDate not supplied

Suppressive effects of central opioids on delayed type hypersensitivity to trinitrochlorobenzene: comparative study with morphine and electroacupuncture.

We reported previously that electroacupuncture (Acu) applied to the acu-point equivalent to GV4 in the mouse just before the 2,4,6-trinitrochlorobenzene (TNCB) challenge suppressed the delayed type hypersensitivity (DTH) through endogenous opioidergic systems in the brain, and the pituitary was pivotal in this immunosuppression. The purpose of the present study was to compare the suppressive effects of Acu with those of single, acute doses of morphine on TNCB-DTH in intact and hypophysectomized (HPX) mice. Subcutaneous morphine 10 mg/kg in ddY mice, 30 mg/kg in BALB/c mice or intracisternal morphine 40 micrograms/mouse in BALB/c mice given just before TNCB challenge suppressed (40-53%) the maximal extent of ear swelling at 24 hrs after challenge in intact mice. In HPX mice, the suppressive effects of intracisternal morphine 10 and 100 micrograms/mouse were less pronounced than those observed in intact mice and there was no significant difference between intact and HPX groups. In addition, suppressive effects observed with Acu or subcutaneous morphine (30 mg/kg) were effectively antagonized by pretreatment with intracisternal naloxone at a dose of as low as 2 micrograms/mouse. Naloxone alone had no effect of its own. These results suggest that 1) the activation of opioid receptor-mediated pathways in the brain, which occurs when opioids are endogenously released (Acu) or exogenously given (morphine), is important in the suppression of TNCB-induced DTH, a cell-mediated immune response, and 2) the pituitary is less pivotal in the suppressive effects of acute morphine than in those of Acu.

Animals↗

PubMedDate not supplied

Induction of apoptotic cell death in human leukemic cell line, HL-60, by extremely low frequency electric magnetic fields: analysis of the possible mechanisms in vitro.

The influence of extremely low frequency electric magnetic fields. (ELF EMFs) on apoptotic cell death was examined using a human leukemic cell line, HL-60 and normal human peripheral blood leukocytes. When HL-60 cells were exposed to 45 mT ELF EMFs, apoptotic cell death, characterized by cell shrinkage, nuclear fragmentation and cleavage of internucleosomal DNA to yield fragments that were multiples of 180-200 base pairs, were induced. The minimum periods required apoptotic HL-60 cell death was 1.0 hour. However, exposure to ELF EMFs could not produce detectable DNA fragmentation in human peripheral blood leukocytes. Static magnetic fields could not induce apoptotic cell death in HL-60 cells, even when the cells were exposed to 180 mT of magnetism for 3.5 hours. We further examined whether hyperthermia induced by induction current in ELF EMFs produced apoptosis in HL-60 cells. Induction current in ELF EMFs enhanced temperature of culture medium to 40.3 degrees C at 3.0 hours of exposure. However, this level of temperature could not induced apoptotic cell death in HL-60 cells, even when cells were cultured for 3.5 hours. These results suggest that induction current produced by ELF EMFs may be one of main mediator in apoptosis in HL-60 cells.

Apoptosis↗

PubMedDate not supplied

Effect of physiological fluids on radical intensity of sodium ascorbate and sodium 5,6-benzylidene-L-ascorbate.

The effect of various physiological fluids on the radical intensity of sodium ascorbate and sodium 5,6-benzylidene-L-ascorbate (SBA) was investigated using ESR spectroscopy. Blood from various animals did not significantly affect the radical intensity of both ascorbates, whereas the corresponding plasma fractions significantly enhanced the radical intensity. This suggests that some populations of blood cells might modify the interaction between plasma components and ascorbates. Saliva contained labile substance(s) which effectively reduced the ascorbate radical intensity. HPLC demonstrated the presence of endogenous ascorbate in rat liver and brain homogenates. When sodium ascorbate or SBA was incubated with any of these homogenates, their radical intensity was synergistically enhanced, but abruptly declined without any apparent ascorbate degradation. Incubation with homogenates elevated the radical intensity of SBA up to the level significantly higher than that of sodium ascorbate. The present data suggest that antitumor action of SBA might be mediated via the accelerated production of ascorbate radical in the target organ.

Animals↗

PubMedDate not supplied

Role of hydrogen peroxide in antitumor activity induction by sodium 5,6-benzylidene-L-ascorbate.

Role of hydrogen peroxide (H2O2) in the induction of antitumor activity against chemically-induced rat hepatocellular carcinoma by sodium 5,6-benzylidene-L-ascorbate (SBA) was investigated. ESR spectroscopy demonstrated that rat liver homogenate of cancerous tissue significantly enhanced the radical intensity of SBA more potently than that of precancerous or normal tissue. The peroxyoxalate chemiluminescence method demonstrated that SBA significantly enhanced the production of H2O2-derived chemiluminescence intensity in the liver homogenates, and the effect of SBA was greater in cancerous tissue than in precancerous or normal tissue. Addition of ascorbic acid, a degradation product of SBA, showed similar but slightly weaker stimulation effects. These data suggest that antitumor activity of SBA in vivo might, at least in part, be due to H2O2 production.

Animals↗

PubMedDate not supplied

Influence of moxibustion on collagen-induced arthritis in mice.

The influence of moxibustion, a traditional Chinese medical treatment; on type II collagen-induced arthritis (CIA) was examined in DBA/1J mice in vivo. Mice were immunized intradermally twice at 3-week intervals with bovine type II collagen (C II). The main incidence of arthritis started around day 30 and lasted to day 60 after the first immunization. Moxibustion, using three different regimens, was applied at the acupoint equivalent to GV4 every other day. Moxibustion, from day 0 to day 30 after the first immunization, suppressed the onset and development of arthritis, as well as anti-collagen antibody level. Treatment with moxibustion, from the day 31 to day 60, also resulted in a significant inhibition of progression of arthritis and production of anti-C II antibody. Furtherfore we examined the influence of moxibustion on the established arthritis. Moxibustion given from day 61 to day 120, mildly but significantly decreased the anti-C II antibody level in diseased mice, while the bone erosion and joint destruction were not affected. These results indicate that moxibustion could prevent the incidence and attenuates the development of murine CIA.

Animals↗

PubMedDate not supplied

Antipyretic action of peripheral stimulation with electroacupuncture in rats.

The present study was designed to investigate the antipyretic action of peripheral stimulation with electroacupuncture (EA) in SD rats. EA stimulation was applied for 30 min to the peripheral muscle where the equivalent Quchi (LI11) acupoint is located. We first examined the effects of EA stimulation on fever induced by either lipopolysaccharide (LPS), interleukin-1 beta (IL-1 beta) or prostaglandin E2 (PGE2). Intraperitoneal injection of LPS at a dose of 100 micrograms/kg caused a high rectal temperature, which was suppressed by EA stimulation. EA stimulation also inhibited the development of fever induced by IL-1 beta injection either intravenously or into the preoptic area (POA). The rats that received administration of PGE2 into POA developed rapid and high fevers, which were attenuated by EA stimulation. In the second part of the experiment, we investigated the levels of cytokines and PGE2 during the development of fever. The concentrations of IL-6 and PGE2 but not IL-1 beta, in brain and serum were increased by intraperitoneal injection of 100 micrograms/kg LPS. EA stimulation reduced PGE2 levels in both brain and serum in LPS-injected rats, but failed to change the levels of IL-6. Intravenous injection of IL-1 beta produced high brain and serum PGE2 levels, which were also significantly suppressed by EA stimulation. The results suggest that EA stimulation possesses an antipyretic effect through the inhibition of the action of PGE2 in rats.

Acupuncture Therapy↗