Characteristics And Outcome Influence Of Increased Plasma Triglyceride Level In Severely Burned Adult Patients.

The aims of this study were to investigate the profile of serum triglyceride level and its influence on outcomes in adult patients with severe burns. An observational study was conducted on 62 patients with burn extent from and over 20% TBSA. Results indicated that serum triglyceride level steadily increased from 1.9mmo/l on the 3rd day to 2.5 mmol/l on the 14th day before reducing on the 21st day after burn. Remarkably higher triglyceride level was seen in patients with full thickness burn area >20% TBSA and in inhalation injury (p < .05). Liver size significantly increased over time and was greater in increased triglyceride patients, but the difference was not significant (p > .05). In addition, patients with elevated serum triglyceride level had significantly higher rates of multiple organ failure and death compared with the remaining group. Further studies need to be conducted to understand and determine intervention for increased plasma triglyceride levels in severely burned patients.

Le but de cette étude était d'évaluer les triglycéridémies et leur influence sur le devenir d'adultes sévèrement brûlés. Il s'agit d'une étude observationnelle réalisée auprès de 62 patients brûlés sur > 20% SCT. La triglycéridémie augmente régulièrement, de 1,9 mmol/L à J3 jusqu'à 2,5 mmol/L à J14 pour diminuer à partir de J21. Des taux particulièrement élevés étaient observés en cas d'atteinte profonde et d'inhalation de fumées (p < 0,05). La taille du foie augmentait au cours du temps et semblait plus élevés chez les patients hypertriglycéridémiques, sans être significative. En outre, les patients hypertriglycéridémiques développaient plus fréquemment une défaillance multiviscérale et leur mortalité était plus élevée. D'autres études sont nécessaires pour comprendre le mécanisme de cette hypertriglycéridémie et proposer une conduite à tenir pour ces patients.

Influence of inhalation injury on resting energy expenditure and plasma metabolic hormones in adult burn patients.

The aim of this study was to investigate the influence of inhalation injury on resting energy expenditure (REE) and some plasma metabolic hormones in adult burn patients. A prospective study was conducted on 16 adult burn patients admitted to the burn intensive care unit, National Burn Hospital, Vietnam. Eight patients with inhalation injury were matched with 8 non-inhalation injury patients by burn extent and age. REE measurements were obtained within 48h of admission and every week after burn. Plasma levels of epinephrine and cortisol were determined on admission and on the 7th day after burns. The results showed that, apart from REE at admission, all values of REE were significantly higher than basal metabolic rate (BMR) at all time points (p < .005). Over time, REE of both groups significantly increased and reached peak values on the 7th day after burn (1964 ± 300Kcal/m2 and 1991.8 ± 467.8Kcal/m2; REE/BMR: 1.5 vs. 1.6 respectively). These values then steadily reduced, but no remarkable differences of REE and REE/BMR were seen between the two groups at any time point (p > .05). In addition, plasma concentrations of epinephrine and cortisol were not significantly different in each group and between the two groups of patients with and without inhalation injury. In conclusion, inhalation injury may not affect metabolic response state in adult burn patients as measured by REE and metabolic hormones.

Le but de ce travail était d'étudier l'influence de l'inhalation de fumées sur la dépense énergétique de repos (DER) et le niveau plasmatique de certaines hormones « métabolique ¼ chez des adultes brûlés. Elle a été réalisée sur 16 patients hospitalisés dans le service de réanimation de l'hôpital brûlologique national du Viêt- Nam, 8 ayant inhalé de la fumée, 8 n'en ayant pas inhalé, appariés sur la surface brûlée. La DER était mesurée dans les 48 h de l'admission puis toutes les semaines. Les taux plasmatiques de cortisol et d'adrénaline étaient mesurés à l'admission et à J7. Mise part celle mesurée à l'admission, DER était systématiquement supérieure à celle calculée selon la formule de Harris- Benedict (p < 0,005), avec un pic à J7 (1964 +/- 300 Cal/m2 chez les patients avec inhalation de fumées, 1991,8 +/- 467,8 chez les autres soit 1,5 et 1,6 fois la DER supposée. Les valeurs mesurées diminuaient ensuite sans jamais qu'il y ait de différence entre les groupes. Pas plus que ne différaient les taux de cortisol ni d'adrénaline. L'inhalation de fumée semble donc de pas avoir d'impact sur la réponse métabolique, mesurée par calorimétrie ou évaluée sur les taux hormonaux.

Diarylheptanoids with free radical scavenging and hepatoprotective activity in vitro from Curcuma longa.

Assay-guided fractionation of the EtOAc soluble fraction of the rhizomes of Curcuma longa furnished three DPPH free radical scavenging diarylheptanoids, curcumin (1), demethoxycurcumin (2), and bisdemethoxycurcumin (3). Compounds 1-3 showed the DPPH radical scavenging effects with IC(50) values of 2.8, 39.2, 308.7 microM, respectively. L-Ascorbic acid and resveratrol as positive controls exhibited IC(50) values of 22.5 and 25.0 microM, respectively. Compounds 1-3 showed significant hepatoprotective effects on tacrine-induced cytotoxicity in human liver-derived Hep G2 cells. The EC(50) values of 1-3 are 86.9, 70.7, and 50.2 microM, respectively. Silybin (EC(50) = 69.0 microM) and silychristin (EC(50) = 82.7 microM) were used as positive controls.

Phosphatidylinositol 3-kinase regulates proliferation of RAW 264.7 macrophages.

Phosphatidylinositol 3-kinase (P13-kinase) is an enzyme that acts as a direct biochemical link between a novel phosphatidylinositol pathway and a number of proteins containing intrinsic or associated kinase activities. Here we demonstrate that wortmannin, P13-kinase inhibitor, decreases the proliferation of RAW 264.7 macrophages and that another structurally unrelated inhibitor of P13-kinase, LY294002. also inhibits the proliferation. These results indicate a possible involvement of P13-kinase in RAW 264.7 macrophages growth regulation. Wortmannin stimulation of RAW 264.7 macrophages is followed by sustained expression of the mRNA of c-fos and a transient expression of the mRNA of c-jun. We also show that the wortmannin and LY294002 induce a cell cycle arrest in asynchronously growing cells leading to an inhibition of cell proliferation after 12 h of treatment. In addition, wortmannin or LY294002 inhibited the phorbol 12-myristate 13-acetate-induced macrophages proliferation potently. These results suggest that P13-kinase plays an important role in growth regulation of RAW 264.7 macrophages and that protein kinase C is a down stream effector of P13-kinase.

Molecular authentication of Panax ginseng species by RAPD analysis and PCR-RFLP.

In order to develop convenient and reproducible methods for the identification of ginseng drugs at a DNA level, randomly amplified polymorphic DNA (RAPD) and PCR-restriction fragment length polymorphism (PCR-RFLP) analyses were applied within Panax species. To authenticate Panax ginseng among ginseng populations, RAPD analysis was carried out using a 20 mer-random primer. The similarity coefficients among the DNA of ginseng plants analyzed were low, ranging from 0.197 to 0.491. In addition, by using PCR-RFLP analysis, very different fingerprints were obtained within Korean ginseng plants. These results suggest that these methods are able to authenticate the concerned Panax species. Broader application of this approach to authenticate other morphologically similar medicinal materials is rationalized.

The activation of PI 3-K and PKC zeta in PMA-induced differentiation of HL-60 cells.

The human myelocytic leukemia cell line HL-60 is a useful model for the study of cellular differentiation. Phorbol 12-myristate 13-acetate (PMA) induces the monocyte/macrophage-like differentiation of HL-60 cells and results in growth arrest, increasing adherence. In PMA-induced differentiation of HL-60 cells, phosphoinositide 3-kinase (PI 3-K) activity was measured as phosphatidylinositol3P recovery from phosphatidylinositol by in vitro kinase assay. PI 3-K activity was increased in HL-60 cells that were stimulated by 20 nM PMA and the activity was inhibited by pretreatment with 20 microM LY294002, a specific inhibitor of PI 3-K. Members of the protein kinase C (PKC) family have been suggested to be one of the downstream targets of PI 3-K. PKC zeta is one of the atypical PKCs, non-diacylglycerol-responsive PKCs, and the activity was measured by the ability of phosphorylation onto myelin basic protein. PMA also induced the activation of PKC zeta during monocytic differentiation of HL-60 cells, and LY294002-pretreated cells failed to induce PKC zeta activation. The activity of PI 3-K is essential for PKC zeta activation, and LY294002 blocks both monocytic differentiation of HL-60 cells and activation of PKC zeta during PMA-induced cell differentiation. This implies that activated PI 3-K subsequently stimulates the PKC zeta in the process of PMA-induced monocytic differentiation.

Significance of ecto-cyclase activity of CD38 in insulin secretion of mouse pancreatic islet cells.

Cyclic ADP-ribose (cADPR), a product of CD38, has a second messenger role for in intracellular Ca(2+) mobilization from microsomes of pancreatic islets as well as from a variety of other cells. ADP-ribosylation of CD38 by ecto-mono ADP-ribosyltransferase in activated T cells results in apoptosis as well as inactivation of its activities. We, therefore, examined the effect of ADP-ribosylation of CD38 in mouse pancreatic islet cells. NAD-dependent inactivation and ADP-ribosylation of CD38, intracellular concentrations of cADPR and Ca(2+), and insulin secretion were measured following incubation of mouse pancreatic islet cells with NAD. ADP-ribosylation of CD38 inactivated its ecto-enzyme activities, and abolished glucose-induced increase of cADPR production, intracellular concentration of Ca(2+), and insulin secretion. Taken together, ecto-cyclase activity of CD38 to produce intracellular cADPR seems to be indispensable for insulin secretion.

Hypoxia induces apoptosis by caspase activation accompanying cytochrome C release from mitochondria in MC3T3E1 osteoblasts. p38 MAPK is related in hypoxia-induced apoptosis.

The aim of this study is to elucidate the possible mechanism of apoptosis in response to hypoxia in MC3T3E1 osteoblasts. MC3T3E1 osteoblasts under hypoxic conditions (2% oxygen) resulted in apoptosis in a time-dependent manner estimated by DNA fragmentation assay and nuclear morphologystained with fluorescent dye, Hoechst 33258. Pretreatment with Z-VAD-FMK, a pan-caspase inhibitor, or Z-DEVD-CHO, a specific caspase-3 inhibitor, completely suppressed the DNA ladder in response to hypoxia. An increase in caspase-3-like protease (DEVDase) activity was observed during apoptosis, but no caspase- activity (YVADase) was detected. To confirm what caspases are involved in apoptosis, western blot analysis was performed using anti-caspase-3 or -6 antibody. The 10-kDa protein, corresponding to the active products of caspase-3 and the 10-kDA protein of the active protein of caspase-6 were generated in hypoxia-challenged cells in which processing of the full length form of caspase-3 and -6 was evident. With a time course similar to this caspase-3 and -6 activation was evident, hypoxic stress caused the cleavage of lamin A, typical of caspase-6 activity. In addition, the stress elicited the release of cytochrome c into the cytosol during apoptosis. Furthermore, we have observed that pre-treatment with SB203580, a selective p38 MAP kinase (p38 MAPK) inhibitor, attenuated the hypoxia-induced apoptosis. The addition of SB203580 suppressed caspase-3 and -6-like protease activity by hypoxia up to 50%. In contrast, PD98059 had no effect on the hypoxia-induced apoptosis. To confirm the involvement of MAP kinase, JNK/SAPK, ERK, or p38 kinase assay was performed. Although p38 MAPK was activated in response to hypoxic treatment, the other MAP kinase -JNK/SAPK or ERK- was not or modestly activated. These results suggest that p38 MAPK positively regulates hypoxia-induced apoptosis in MC3T3E1 osteoblasts.

Kunbi-Boshin-Hangam-Tang stimulates nitic oxide production through activation of nuclear factor-kappaB.

The objective of the currently study was to determine the effect of Kunbi-Boshin-Hangam-Tang (KBH-Tang) on the production of nitric oxide (NO). Stimulation of RAW 264.7 cells with KBH-Tang after the treatment of recombinant interferon-gamma (rIFN-gamma) resulted in increased NO synthesis. KBH-Tang partially increased NO synthesis by itself. When KBH-Tang was used in combination with rIFN-gamma, there was a marked cooperative induction of NO synthesis in a dose-dependent manner. This increase in NO synthesis was reflected as increased amount of inducible NO synthase (iNOS) protein. NO production was inhibited by NG-monomethyl-L-arginine (NGMMA). Furthermore, activation of nuclear factor (NF)-kappaB was increased by KBH-Tang. These results suggest that KBH-Tang may stimulate the NO production through the activation of the NF-kappaB.

Cyclic-AMP inhibits nitric oxide-induced apoptosis in human osteoblast: the regulation of caspase-3, -6, -9 and the release of cytochrome c in nitric oxide-induced apoptosis by cAMP.

Nitric oxide (NO) induces apoptotic cell death and cAMP has a significantly protective effect on NO-induced cytotoxicity in human osteoblasts, MG-63 cells. Treatment with S-nitroso-N-acetylpenicillamine (SNAP) (0.6 mM) resulted in genomic DNA fragmentation, characteristic of apoptosis. However, concomitant incubation of the cells with either DBcAMP or forskolin markedly inhibited SNAP-induced apoptosis in a dose-dependent manner. Furthermore, pretreatment of MG-63 cells with H-89 or KT5720, which is known to inhibit cAMP-dependent protein kinase (PKA), abolished the protective effect of DBcAMP and forskolin on SNAP-induced apoptosis. In this study, we explored the involvement of caspases in the regulatory mechanism of SNAP-induced apoptosis by cAMP. Our data show that DBcAMP or forskolin blocked SNAP-induced caspase-3-like cysteine protease activation and that H-89, a PKA inhibitor, reversed the cAMP-induced regulatory effect of caspase-3 like protease. Consistent with the results, cAMP inhibited the proteolytic cleavage of caspase-3, -6, -9 and cytochrome c release to cytoplasm. The inhibition of caspase-3 activation did not block SNAP-induced cytochrome c release to cytoplasm, suggesting that caspase-3 activation may occur downstream of cytochrome c release. In summary, these findings show that the exposure of MG-63 cells to cAMP analogs renders them more resistant to NO-induced damage and suggests the presence of regulatory mechanisms of the cell death pathway by cAMP in which caspase-3, -6, and -9 and cytochrome c release serves to mediate NO-induced apoptosis.

Polymorphism of the angiotensin-converting enzyme gene in patients with cerebral infarction in Koreans.

The relationship between cerebrovascular disease and an insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene is still being debated. The frequency of the DD genotype of the ACE gene was significantly higher in subjects with than those without cerebral infarction in Japan. The aim of the present study was to assess the relationship between ACE gene polymorphism and the development of cerebral infarction in a population from Korea. We examined its possible role as a risk factor in patients with cerebral infarction. The association between ACE gene polymorphism and cerebral infarction was examined in 106 patients with cerebral infarction and 498 controls without cerebral infarction. Frequencies of the genotypes and alleles of the ACE gene were investigated. The ACE genotype was analyzed by the polymerase chain reaction (PCR). The frequency of D allele was 37.7% in patients and 39.1% in controls (chi2 = 0.128, p = 0.720). The frequencies of the genotypes of the ACE gene were II: 39.6%, ID: 45.3%, and DD: 15.1% in patients, and II: 37.1%, ID: 47.6%, and DD: 15.3% in controls (chi2 = 0.127, p = 0.721). There was no significant difference in the frequency of the DD genotype of the ACE gene, and we did not find any association between ACE polymorphism and cerebral infarction. These results indicate that ACE polymorphism is not a risk factor for the development of cerebral infarction in a Korean population.

Inhibition of tumor necrosis factor-alpha-induced apoptosis by Asparagus cochinchinensis in Hep G2 cells.

A human hepatoma cell line, Hep G2 cells, is a reliable system for the study of alcohol-induced hepatotoxicity. In this study, we investigated the effect of an aqueous extract of Asparagus cochinchinensis(MERRIL) (Liliaceae) roots (ACAE) on ethanol (EtOH)-induced cytotoxicity in Hep G2 cells. ACAE (1-100 microg/ml) dose-dependently inhibited the EtOH-induced tumor necrosis factor-alpha (TNF-alpha) secretion. ACAE (1-100 microg/ml) also inhibited the EtOH and TNF-alpha-induced cytotoxicity. Furthermore, we found that ACAE inhibited the TNF-alpha-induced apoptosis of Hep G2 cells. These results suggest that ACAE may prevent the EtOH-induced cytotoxicity through inhibition of the apoptosis of Hep G2 cells.

Effect of Vitex rotundifolia on immediate-type allergic reaction.

We investigated the effect of aqueous extract of Vitex rotundifolia (L.) (Verbenaceae) fruits (VRFE) on the immediate-type allergic reactions in vivo and in vitro. VRFE (10(-4)-1.0 g/kg) dose-dependently inhibited systemic allergic reaction induced by compound 48/80. When VRFE was employed in a systemic allergic reaction test, the plasma histamine levels were reduced in a dose-dependent manner. VRFE (5x10(-1) and 1.0 g/kg) inhibited passive cutaneous anaphylaxis activated by anti-dinitrophenyl (DNP) IgE. VRFE (10(-3)-1.0 mg/ml) also dose-dependently inhibited the histamine release from the rat peritoneal mast cells (RPMC) by compound 48/80 or anti-DNP IgE. Moreover, VRFE (10(-3) mg/ml) had a significant inhibitory effect on anti-DNP IgE-induced tumor necrosis factor-alpha production from RPMC. These results suggest that VRFE may be beneficial in the regulation of immediate-type allergic reaction.

Taraxacum officinale inhibits tumor necrosis factor-alpha production from rat astrocytes.

Substance P (SP) can stimulate production of tumor necrosis factor-alpha (TNF-alpha) from astrocytes stimulated with lipopolysaccharide (LPS). The objective of the current study was to determine the effect of Taraxacum officinale (TO) on the production of TNF-alpha from primary cultures of rat astrocytes. TO (100 and 1000 microg/ml) significantly inhibited the TNF-alpha production by astrocytes stimulated with LPS and SP. Interleukin-1 (IL-1) has been shown to elevate TNF-alpha production from LPS-stimulated astrocytes while having no effect on astrocytes in the absence of LPS. We therefore examined whether IL-1 mediated inhibition of TNF-alpha production from primary astrocytes by TO. Treatment of TO (100 and 1000 microg/ml) to astrocytes stimulated with both LPS and SP decreased IL-1 production significantly. Moreover, the production of TNF-alpha by LPS and SP in astrocytes was progressively inhibited with increasing amount of IL-1 neutralizing antibody. Our results suggest that TO may inhibit TNF-alpha production by inhibiting IL-1 production and that TO has an antiinflammatory activity in the central nervous system.

Inhibitory effect of mast cell-mediated immediate-type allergic reactions by sulfapyridine.

We examined the effect of sulfapyridine on mast cell-mediated immediate-type allergic reactions. Sulfapyridine (1 and 10 microg/kg) significantly inhibited systemic allergic reaction induced by compound 48/80 in rats. Sulfapyridine (1 and 10 microg/kg) also inhibited significantly local mast cell-mediated immediate-type allergic reactions activated by anti-dinitrophenyl (DNP) IgE. Moreover, sulfapyridine inhibited histamine release dose-dependently in the rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti-DNP IgE. When sulfapyridine was added, the level of cAMP in RPMC, transiently and significantly increased about 4-fold compared with that of basal cells. These results indicate that sulfapyridine inhibits mast cell-mediated immediate-type allergic reactions in vivo and in vitro.

Inhibitory effect of sodium salicylate on nitric oxide production from TM4 sertoli cells.

Nitric oxide (NO) has been proposed to play a role in a variety of inflammatory diseases. Sodium salicylate (NaSal) is the most commonly used anti-inflammatory agent. We investigated whether NaSal can diminish the production of NO in TM4 Sertoli cells. TM4 Sertoli cells produced a small amount of NO upon treatment with recombinant interferon-gamma (rIFN-gamma). The effect of rIFN-gamma was enhanced markedly by the addition of recombinant TNF-alpha (rTNF-alpha) in a dose-dependent manner. NaSal (10 and 20 mM) significantly inhibited NO production from TM4 Sertoli cells induced by rIFN-gamma plus rTNF-alpha. In addition, rIFN-gamma in combination with rTNF-alpha showed a marked increase of the expression of inducible NO synthase (iNOS) protein. Western blot analysis revealed that NaSal (10 and 20 mM) blocked a step of iNOS protein synthesis. The rIFN-gamma plus rTNF-alpha-induced nuclear factor-kappaB (NF-kappaB) activation was significantly blocked by NaSal (10 and 20 mM). On the other hand, neither staurosporine nor polymyxin B significantly inhibited NO production from TM4 Sertoli cells induced by rIFN-gamma plus rTNF-alpha. The present results indicate that NaSal inhibits rIFN-gamma plus rTNF-alpha-induced NO production in TM4 Sertoli cells via the signal transduction pathway of NF-kappaB activation.

Inhibitory effect of anaphylactic shock by caffeine in rats.

Caffeine is known to reduce evoked histamine secretion, but the effects of caffeine on anaphylactic shock have not been clarified. We have investigated the effects of caffeine on anaphylactic shock in rats. Systemic anaphylactic shock by compound 48/80 injection was monitored for 1 h. An IgE-dependent local anaphylactic shock was generated by sensitizing the skin with anti-dinitrophenyl (DNP) IgE followed 48 h later with an injection of antigen. Caffeine inhibited compound 48/80-induced anaphylatic shock to 40% with a dose of 1 mg/kg. Caffeine (0.1 mg/kg) inhibited to 56.4+/-0.4% passive cutaneous anaphylactic shock activated by anti-DNP IgE. Caffeine (5-20 mM) significantly inhibited histamine release from rat peritoneal mast cells (RPMCs) activated by compound 48/80 or anti-DNP IgE. Especially, caffeine (20 mM) inhibited by 96.7+/-0.5% histamine release activated by compound 48/80. Moreover, caffeine (1-20 mM) had a significant inhibitory effect on anti-DNP IgE-induced tumor necrosis factor-alpha production from RPMCs. The level of cAMP in RPMCs, when caffeine (20 mM) was added, increased significantly after 5-60 min compared with that of a normal control. These results indicate that caffeine inhibits immediate-type allergic reactions by inhibition of mast cell degranulation in vivo and in vitro.

Protein kinase C independent activation of inducible nitric oxide synthase by tumor necrosis factor-alpha in TM4 Sertoli cells.

To investigate the nitric oxide (NO) production and its signalling mechanism in TM4 Sertoli cells, the cells were treated with recombinant tumor necrosis factor-alpha (rTNF-alpha), recombinant interleukin-1 alpha (rIL-1alpha), or lipopolysaccharide (LPS), either alone or in combination with recombinant interferon-gamma (rIFN-gamma), and NO production was measured by using the Griess method. TM4 Sertoli cells produced a small amount of NO upon treatment with rIFN-gamma. The effect of rIFN-gamma was drastically increased by cotreatment with rTNF-alpha in a dose-dependent manner. However, combination of rIL-1alpha or LPS with rIFN-gamma did not synergize to activate cells. RIFN-gamma in combination with rTNF-alpha showed marked increase of the expression of iNOS protein. Protein kinase C inhibitors did not inhibit the production of NO induced by rIFN-gamma plus rTNF-alpha. These results suggest that the role of TNF-alpha is to provide TM4 Sertoli cells with the active cofactor for NO production and TNF-alpha-induced signaling for induction of NO synthesis is not dependent on protein kinase C activation.

Action of Sosiho-Tang on systemic and local anaphylaxis by anal administration.

The herbal formulation Soshiho-Tang (SS-Tang) has been used against allergic disease for generations, and still occupies an important place in traditional medicine in Korea. Previously, we reported that SS-Tang potently inhibited mast cell- mediated anaphylaxis when orally administered. In this study, we investigated the effect of SS-Tang by anal administration in anaphylaxis responses. SS-Tang dose-dependently inhibited compound 48/80-induced systemic anaphylaxis with doses of 10(-4) to 1 g/kg 1 h before anally administered. Of special note, SS-Tang inhibited systemic anaphylaxis completely with a dose of 1 g/kg. SS-Tang reduced plasma histamine levels induced by compound 48/80 significantly. However, the mortality was 100% when SS-Tang was administered after compound 48/80 treatment. SS-Tang (10(-1) g/kg) also inhibited passive cutaneous anaphylaxis activated by anti-dinitrophenyl IgE antibody by 30.9%. These results provide evidence that anal therapy of SS-Tang may be beneficial in the treatment of systemic and local anaphylaxis.

Interleukin-3 or immunoglobulin E promotes expression of protein kinase C delta gene in murine mast cells.

We reported previously that protein kinase C delta (PKCdelta) is the main isoenzyme in various types of murine mast cells. In the present study we investigated the regulation of expression of PKCdelta gene in murine mast cells in vitro and in vivo. The mRNA expressions of PKCdelta were promoted in response to interleukin-3 (IL-3) or immunoglobulin E (IgE) in mouse mastocytoma P-815 cells. In addition we have evaluated the mast cells which express PKCdelta mRNA in IgE-dependent passive cutaneous anaphylaxis reaction, using in situ hybridization with the antisense riboprobe in skin. These results indicate that mast cell activation can induce a marked promotion in steady state levels of PKCdelta mRNA.