Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DEXAMETHASONE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,153 records · Page 64Linked to original sources
PubMed1983

Regulation of neurotensin secretion in a mammalian C cell line: effect of dexamethasone.

We established in culture two colony clones of rMTC 44-2 cells, rMTC 44-2B and 44-2C which secrete substantially greater quantities of neurotensin (NT) than the parent cell line. We describe here the effects of the synthetic glucocorticoid, dexamethasone, on NT and cAMP release. Medium and intracellular levels of NT and cAMP were measured by specific RIAs. Long-term release experiments were performed in Dulbecco's Modified Eagle's Medium supplemented with 15% horse serum (DMEM). Short-term release experiments were performed in Krebs-Ringer-bicarbonate-glucose buffer (KRBG) supplemented with 1.0 mm Ca2+. Dexamethasone stimulated NT release and increased intracellular NT levels. The ED50 values for stimulation of NT release following 24 or 48 h incubation of cells in DMEM with dexamethasone were 5 X 10(-9) and 7 X 10(-9) M, respectively. Dexamethasone markedly enhanced intracellular levels of NT in rMTC 44-2 cells while it decreased cell growth. Cells pretreated with dexamethasone for 48 h released greater amounts of NT in response to Ca2+ (1.0 mM) with or without K+ (50 mM) or NE (10(-6) M) following a 10 min incubation with these substances in KRBG. This experimental paradigm was also used to measure the efflux of cAMP following a brief (10 min) exposure of cells to NE. We conclude that the rMTC 44-2B and 44-2C cells are useful tools for studying the effects of dexamethasone on the regulation of cell growth, as well as the secretion of NT and cAMP.

Animals↗
PubMed1993

Induction of peroxisomal acyl-CoA oxidase by 3-thia fatty acid, in hepatoma cells and hepatocytes in culture is modified by dexamethasone and insulin.

The effects of tetradecylthioacetic acid (TTA) (50 microM), dexamethasone (0.25 microM) and insulin (0.4 microM) on induction of peroxisomal acyl-CoA oxidase activity and mRNA levels were studied in short term cultures of Morris 7800C1 and MH1C1 hepatoma cells and of rat hepatocytes. Dexamethasone and TTA resulted in parallel increases in the enzyme activity and the steady state mRNA content in the hepatoma cells. Combination of dexamethasone and TTA resulted in a synergistic and parallel stimulation of both the enzyme activity and the mRNA levels up to 11-12-fold and maximal changes were observed after 14 days of treatment. Semiquantitative immunoblot analyses of acyl-CoA oxidase were in concordance with enzyme and mRNA results. Insulin counteracted the inductive effects of dexamethasone and TTA on all parameters. The half-life of the acyl-CoA oxidase mRNA increased after treatment with the 3-thia fatty acid (t1/2 = 10.0 h +/- 0.4) compared to control (t1/2 = 5.9 h +/- 0.3). However, in combination with dexamethasone there was no further increase in the mRNA stability (t1/2 = 8.0 h +/- 0.3). Southern blot analysis did not reveal any changes on the oxidase gene level in any treatment group. TTA alone or in combination with dexamethasone did not affect the expression of either the glucocorticoid receptor or the peroxisomal proliferator acting receptor (PPAR) steady state mRNA levels. In cultured hepatocytes the acyl-CoA oxidase was modified in similar manner by these treatments, but the changes were less marked. We suggest that the changes in peroxisomal acyl-CoA oxidase activity in hepatoma cells are due to a major effect on the level of mRNA, involving both transcriptional effects and message stabilization.

Acyl-CoA Oxidase↗
PubMed1987

The effect of dexamethasone, insulin and triiodothyronine on microsomal NADPH-cytochrome-c (P-450) reductase in primary cultures of isolated hepatocytes.

NADPH-cytochrome-c (P-450) reductase, a flavoprotein, is a constituent of the hepatic microsomal polysubstrate monooxygenase and catalyzes the transfer of electrons from NADPH to cytochrome P-450. The hormonal regulation of NADPH-cytochrome-c reductase activity and protein has been examined in insolated hepatocytes cultured as monolayers for 48 h in Waymouth's MB752/1 medium fortified with insulin, dexamethasone and triiodothyronine. No similarity between the response of NADPH-cytochrome-c reductase and of tyrosine aminotransferase and malate dehydrogenase activity to dexamethasone and triiodothyronine treatment could be detected. In the absence of hormones about 65% of the original NADPH-cytochrome-c reductase activity and protein estimated by the immunochemical staining technique was retained. Culture of hepatocytes in insulin (10.0 mU/ml) or dexamethasone (100 nM) alone but not triiodothyronine improved the retention of reductase activity and protein. Only when hepatocytes were cultured in insulin, triiodothyronine and dexamethasone could NADPH-cytochrome-c reductase activity and protein be maintained at the original level. Dexamethasone alone was found to enhance consistently retention of reductase protein, but not reductase activity, to approximately the same level as in freshly isolated hepatocytes. The results suggest that microsomal NADPH-cytochrome-c reductase activity and protein can be maintained in isolated hepatocytes at the original level by culturing the cells in dexamethasone, insulin and triiodothyronine.

Animals↗
PubMed1985

Suppression of phagocytosis by dexamethasone in macrophage cultures: inability of arachidonic acid, indomethacin, and nordihydroguaiaretic acid to reverse the inhibitory response mediated by a steroid-inducible factor.

Glucocorticoid steroids inhibit phagocytosis and cell spreading in cultures of murine resident peritoneal macrophages. It is postulated that these suppressive responses are mediated by a steroid-induced substance elaborated from dexamethasone-treated macrophages. Accordingly, dialyzed medium from dexamethasone-treated cultures was analyzed for the presence of a factor that inhibits phagocytosis and cell spreading in macrophage cultures not exposed to the steroid. When previously untreated macrophages were supplied dialysates from steroid-treated cultures, cell spreading and the phagocytic capacity (i.e. percentages of phagocytes in macrophage populations and the ability of phagocytes to ingest heat-killed Saccharomyces cerevisiae particles) decreased dramatically between 2 and 24 h after exposure. A lesser transient inhibitory response was observed when dialysates from untreated cultures were used. Relative to these controls after 48 h, phagocytic capacity and cell spreading remained suppressed in cultures treated with dialysates from dexamethasone-treated cultures. The addition of arachidonate, in the absence and presence of cyclooxygenase and lipoxygenase inhibitors, did not affect the phagocytic capacity of control macrophages. Furthermore, the addition of these compounds, either alone or in combination, to dexamethasone-treated cultures did not modulate the steroid-induced suppression of phagocytosis. These results support the hypothesis that the inhibition of phagocytosis and cell spreading may be mediated by a dexamethasone-induced non-dialyzable factor. In addition, the inability of arachidonic acid and inhibitors of prostaglandin and leukotriene biosynthesis to reverse the steroid-induced suppression of phagocytosis implies that the inhibition of this important macrophage function is not associated with the failure of dexamethasone-treated macrophages to release these mediators.

Animals↗
PubMed1995

Effects of nicotinamide on hepatocyte viability and secretion of albumin and alpha 1-acid glycoprotein by adult rat hepatocytes in primoculture. Comparison with dexamethasone and recombinant human interleukin-6.

The effects of nicotinamide on hepatocyte viability and secretion of albumin and alpha 1-acid glycoprotein were studied in the absence or presence of dexamethasone and/or recombinant human interleukin-6 either after cell attachment (2 h) or after 24, 48, and 72 h of culture. The evolution of hepatocyte survival during the culture was appreciated by measurement of total DNA content. The secretion of albumin and alpha 1-acid glycoprotein was measured after a 4-h period following cell attachment or after 24, 48 and 72 h of culture. The important decrease of DNA content, mRNA levels and secretion of albumin and alpha 1-acid glycoprotein in control cultures after 2-3 days was not prevented by the addition of nicotinamide. In contrast, dexamethasone alone or with recombinant human interleukin-6 improved DNA content and albumin secretion with no additional effect of nicotinamide. The secretion of alpha 1-acid glycoprotein was largely induced by dexamethasone alone or dexamethasone and recombinant human interleukin-6. The increase of alpha 1-acid glycoprotein secretion was not modified by the addition of nicotinamide and averaged respectively 27- and 60-fold for dexamethasone alone and dexamethasone and recombinant human interleukin-6 after 48 h. These observations suggested that nicotinamide, at least in the conditions tested here, is unable to prevent alterations of hepatocyte viability and gene expression of cultured hepatocytes.

Animals↗
PubMed1983

The effect of prenatal dexamethasone on fetal rat lung prostaglandin synthesis.

[14C]Arachidonic acid conversions were studied in homogenates of lungs from 20, 21, and 22 day fetuses with or without prenatal dexamethasone treatment. The major metabolites were in all cases 12-L-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HETE), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), prostaglandin E2 (PGE2), and 12-L-hydroxy-5,8,10-heptadecatrienoic acid (HHT). Prostaglandin F2 alpha (PGF2 alpha), prostaglandin D2 (PGD2), and thromboxane B2 (TxB2) were present in small amounts. Dexamethasone treatment significantly stimulated the conversion of [14C]-arachidonic acid in fetal lung homogenates to 6-keto-PGF1 alpha, PGE2, 12-HETE, and HHT, at 20 days gestational age. This effect was dependent on the dose of dexamethasone. These results suggest that dexamethasone accelerates the maturation of the enzymes involved in prostaglandin synthesis. Because dexamethasone is also known to inhibit phospholipase A2, further studies are required to determine the overall in vivo effect of prenatal dexamethasone therapy on fetal lung prostaglandin synthesis.

Animals↗
PubMed1988

A randomized trial of oral nabilone and prochlorperazine compared to intravenous metoclopramide and dexamethasone in the treatment of nausea and vomiting induced by chemotherapy regimens containing cisplatin or cisplatin analogues.

Eighty patients receiving their first course of chemotherapy with regimens containing cisplatin or cisplatin analogues entered this open crossover study comparing nabilone 2 mg and prochlorperazine 5 mg given orally every 12 h for four doses against metoclopramide 2 mg/kg loading dose intravenously (i.v.), then 3 mg/kg as an (i.v.) infusion over 8 h and dexamethasone 20 mg (i.v.) over 3-5 min at the time of chemotherapy. There was complete control of nausea and vomiting in 24 patients (32%) given metoclopramide and dexamethasone compared to 14 patients (19%) given nabilone and prochlorperazine. For the 70 patients who completed the crossover assessment of emesis on a linear analogue scale significantly favoured metoclopramide and dexamethasone (P = 0.02). However, there was no overall patient preference for the metoclopramide and dexamethasone combination (nabilone and prochlorperazine 31 vs. metoclopramide and dexamethasone 26; 13 no preference), because a significant proportion of the patients receiving the cisplatin analogue carboplatin preferred nabilone and prochlorperazine (16 vs. 5; 1 no preference; P = 0.013). For patients receiving cisplatin chemotherapy metoclopramide and dexamethasone remains the antiemetic of choice but for regimens containing carboplatin, nabilone and prochlorperazine is better tolerated and preferred by the patients.

Adolescent↗
PubMed1989

Dexamethasone control of growth hormone mRNA levels in GH3 pituitary cells is cycloheximide-sensitive and primarily posttranscriptional.

To clarify the mechanism of growth hormone (GH) gene activation by glucocorticoids in GH3 pituitary cells, GH mRNA accumulation in nuclear and cytoplasmic compartments was measured in the presence and absence of cycloheximide. In dexamethasone-treated cells, levels of GH mRNA were increased in the nucleus by 6 h and in the cytoplasm by 12 h. Dexamethasone treatment caused a 5- to 24-fold rise in total GH mRNA levels by 48-72 h. The differential elevation of nuclear levels of GH mRNA relative to the amount of cytoplasmic GH mRNA persisted for 48 h. A transient accumulation of GH mRNA in the nucleus was followed by a brief rise in cytoplasmic GH mRNA levels in GH3 cells treated simultaneously with dexamethasone and cycloheximide. In GH3 cells pretreated for 2 h with cycloheximide, the rise in nuclear and cytoplasmic GH mRNA levels mediated by dexamethasone was blocked completely. Levels of glucocorticoid receptor were unaffected by cycloheximide. These data suggest that the stimulation of GH mRNA levels by glucocorticoids is initiated within the nucleus and that cycloheximide-sensitive events are essential for this stimulation to occur. To assess the importance of GH gene transcriptional activation by glucocorticoids, nuclear transcription run-on reactions and assays of GH promoter activity in an aminoglycoside 3'-phosphotransferase (Neo) fusion gene within stably transformed GH3 cells were performed. Evidence for a weak, transient transcriptional activation of the GH gene by dexamethasone in nuclear run-on assays was obtained. Consistent with this idea, a 30-72 h exposure to dexamethasone raised levels of Neo mRNA in GH-Neo GH3 cell transformants by less than or equal to 2-fold. We conclude that glucocorticoid stimulation of GH mRNA in GH3 cells requires ongoing protein synthesis and can occur largely independently of GH gene transcriptional activation.

Animals↗
PubMed1989

The influence of dexamethasone on serum thyrotrophin and thyrotrophin synthesis in the rat.

Glucocorticoid hormones suppress circulating concentrations of thyrotrophin (TSH), but their effect on synthesis of TSH in the pituitary gland is unclear. We have examined the influence of the glucocorticoid dexamethasone on serum TSH, pituitary TSH content and TSH beta- and alpha-subunit mRNA concentrations in pituitary cytoplasm in both the euthyroid and hypothyroid rat, and following triiodothyronine (T3) treatment in the hypothyroid rat. The rise in serum TSH in hypothyroidism was attenuated in animals treated with dexamethasone; in addition the suppression of serum TSH 6 h after T3 administration to hypothyroid rats was enhanced by dexamethasone. In contrast to the changes in serum TSH, pituitary TSH content was unaffected by dexamethasone. Furthermore dexamethasone had no significant effect on changes in pituitary cytoplasmic TSH beta- and alpha-subunit mRNA levels with thyroid status. These findings demonstrate that dexamethasone exerts differential effects on serum TSH levels and TSH biosynthesis which contrast with those of thyroid hormones.

Animals↗
PubMed1993

Dexamethasone stimulates rRNA gene transcription in rat myoblasts.

The glucocorticoid analogue, dexamethasone, stimulated RNA synthesis more than two-fold in rat L6 myoblasts, without affecting the rate of cell proliferation. Treatment of myoblasts for 24 h with 10(-7) M dexamethasone resulted in a 30% increase in the cellular RNA level. More than a two-fold stimulation of pre-rRNA gene transcription by dexamethasone, as measured in isolated nuclei and by cell-free transcription, was accompanied by a corresponding increase in pre-rRNA levels. Co-incubation of myoblasts with cycloheximide and dexamethasone did not affect the enhanced pre-rRNA gene transcription demonstrating that de novo protein synthesis was unnecessary to manifest the dexamethasone effect on rDNA transcription. Support for this conclusion is provided by the finding that the levels of UBF1 and UBF2, rDNA upstream binding transcription factors, remain unchanged. The glucocorticoid antagonist RU38486 [11 beta-(4-dimethylaminophenyl)17 beta-hydroxy-17 alpha-(prop-1-ynyl)estra- 4,9-dien-3-one] inhibited the dexamethasone-stimulated rRNA gene transcription suggesting that the glucocorticoid receptor is involved in the response mechanism.

Animals↗
PubMed1995

Effects of dexamethasone on the epiplexus cells in postnatal rats.

The epiplexus cells in postnatal rats were markedly reduced in number and immunoreactivity for OX-42, OX-18 and ED1 following subcutaneous injections of dexamethasone. This was especially evident in rats receiving two or three successive injections of dexamethasone and killed at the age of 4 or 7 days. At 14 and 21 days, the cells did not exhibit any striking difference from their corresponding controls in terms of cell number and immunoreactivity for the above antibodies. Occasional epiplexus cells were labelled with the antibody OX-6 in both groups of rats sacrificed at different time points. In rats receiving dexamethasone coupled with rhodamine isothiocyanate (RhIc), the epiplexus cells, though fewer in number than the corresponding controls, emitted bright fluorescence. It is concluded that the reduction of epiplexus cells following dexamethasone injections is due to the suppression of their precursor cells, i.e. monocytes. The phagocytic activity of the persisting epiplexus cells did not appear to be abolished by dexamethasone as evidenced by their uptake of RhIc. Our results suggest that the effects of dexamethasone are reversible.

Animals↗
PubMed1991

The action of dexamethasone on electrically-induced contractions of guinea-pig isolated ileum.

1. The effect of dexamethasone and its interaction with morphine has been studied on transmurally-stimulated guinea-pig ileum preparation. 2. Dexamethasone dose-dependently depressed the contractions of the ileum; this action has a rapid onset. 3. Naloxone did not reverse the inhibitory effect of dexamethasone. 4. When dexamethasone and morphine were given in combination the maximum reduction observed was equal to the sum of the single effect of two drugs given individually and naloxone antagonized only the inhibition induced by morphine. 5. Proteic synthesis inhibitors did not modify the inhibition induced by dexamethasone. 6. RU-38486, a glucocorticoid antagonist receptor, antagonized completely the inhibitory effect of DXM without affecting the inhibition induced by morphine showing that the effect of dexamethasone occurs by glucocorticoid receptor-mediated processes.

Animals↗
PubMed1992

Dexamethasone modifies morphine-, atropine-, verapamil-induced constipation in mice.

1. The effect of dexamethasone in gastrointestinal constipation induced by morphine, verapamil and atropine in mice has been studied. 2. These drugs caused a dose-related inhibition of charcoal meal transit, which was reversed by dexamethasone. 3. Dexamethasone resulted more active in reversing morphine and atropine constipation, than in modifying verapamil effect. 4. The authors concluded that the interaction of dexamethasone on its receptor could release a larger amount of acetylcholine resulting in a reversion of atropine- or morphine-induced constipation. 5. The minor effect of dexamethasone on verapamil-induced constipation suggest a reduced involvement of calcium influx. 6. The above results suggest a role for steroid in gastrointestinal transit and propose a possible mechanism through which dexamethasone could reverse morphine- and atropine-induced constipation.

Animals↗
PubMed1984

Comparison of plasma cortisol and corticosterone in the dexamethasone suppression test for melancholia.

The suppression of plasma corticosterone (B), measured by radioimmunoassay (RIA), was compared to simultaneous suppression of plasma cortisol (F), measured as total corticoids by a competitive protein binding (CPB) assay, in the overnight dexamethasone suppression test (DST). Baseline plasma B concentrations in 10 control subjects were 4.04 +/- 1.07 ng/ml (X +/- S.D.) at 0800 hr and 1.51 +/- 0.68 ng/ml at 1600 hr. Post-dexamethasone 1600 hr B levels in the controls were 0.46 +/- 0.29 ng/ml. An early escape of plasma B (greater than 1.2 ng/ml), like that of F (greater than 5 micrograms/dl), during the overnight 24 hr 1.0 mg dose DST was noted in patients with melancholia (endogenous depression). Half-hourly catheter samples in a normal subject stimulated to escape from dexamethasone suppression showed that in general, plasma B concentrations parallel plasma F concentrations over a 12 hr period. Repeated weekly DSTs on two patients with different psychiatric diagnoses resulted in B : F correlations of 0.74 and 0.60. Overall agreement between B- and F-DST outcomes in all categories tested at 1600 and 2300 hr was 93%; the agreement in the melancholic and non-endogenous depressed groups was 100%. Post-dexamethasone, both B and F were suppressed 55-60% below the criterion level in controls. In those patients who escaped from dexamethasone suppression, the percentage increase in plasma B above the criterion level was significantly greater (+55%) than the corresponding percentage change in plasma F. Most patients with borderline abnormal F-DSTs (3.5 - 4.9 micrograms/dl) exhibited clearly abnormal B-DSTs (greater than 1.2 ng/ml). We conclude that the use of dexamethasone suppression of plasma B (using 1.2 ng/ml as the abnormal criterion value) is an additional indicator of an abnormal DST in depressed patients.

Bipolar Disorder↗
PubMed1987

The dexamethasone and cortisol suppression test in depression: beta-endorphin as a useful marker.

To investigate the mechanism underlying disturbances in hypothalamopituitary-adrenal (HPA) function in depressed patients, the dexamethasone suppression test (DST) was compared with a cortisol suppression test (CST) and placebo treatment in depressed patients and control subjects. Plasma levels of cortisol, ACTH and beta-endorphin were assessed at 3 times during the day after treatment with a single dose of exogenous steroid. Both dexamethasone and cortisol treatment resulted in suppression of cortisol, ACTH and beta-endorphin in control subjects, while neither treatment had any effect on the hormone levels in those depressed patients who showed cortisol nonsuppression after dexamethasone. In the depressed patients who were cortisol suppressors after dexamethasone, cortisol treatment only slightly changed plasma levels of beta-endorphin, although they were suppressed after dexamethasone treatment. In addition, high levels of both cortisol and beta-endorphin were observed after placebo treatment in all depressed patients compared to control subjects, probably due to the absence of the normally occurring decrease of these hormones during the day in these patients. Cortisol treatment, but not dexamethasone treatment, discriminated depressed patients from controls with respect to their beta-endorphin plasma levels. However, it is not yet clear whether these different effects of the two steroids are related to a different mode of action of these steroids in depressed patients. beta-Endorphin seems to be a useful marker in detecting disturbances in HPA function among depressed patients.

Adrenocorticotropic Hormone↗
PubMed1988

Effect of dexamethasone on cortisol and prolactin responses to meals in bulimic and normal women.

In normal individuals, serum cortisol and prolactin concentrations have been shown to rise following a mid-day meal. To determine whether abnormalities of the hypothalamo-pituitary-adrenal axis in bulimics lead to a disrupted hormonal response to eating, cortisol and prolactin responses to meals (600 kcal, 30% protein, 30% fat, 40% carbohydrate) were studied on two consecutive days in six normal weight bulimics and six normal volunteers. Dexamethasone (1 mg orally) was administered at 2330 h after baseline sampling. During baseline sampling, cortisol concentrations were significantly higher in the bulimics (18.2 +/- 0.9 micrograms/dl, mean +/- SEM) than in the normals (12.1 +/- 0.4 micrograms/dl) (p less than 0.001). Post-dexamethasone cortisol concentrations also were higher in the bulimics (5.7 +/- 0.3 micrograms/dl) than in the normals (1.2 +/- 0.2 micrograms/dl) (p less than 0.001). The three bulimics with a major depressive disorder had higher peak post-dexamethasone cortisol concentrations than the nondepressed bulimics. Dexamethasone significantly enhanced the prolactin response to meals among both bulimics (at 90 min post onset of eating) and normals (at 60, 75 and 90 min post onset of eating). This enhancement of the prolactin response to meals by dexamethasone is opposite to the inhibitory effect of dexamethasone on stress-induced prolactin release and suggesting that stress-induced and meal-induced prolactin release involve different neuroendocrine mechanisms.

Adult↗
PubMed1993

Respiratory status and diuresis following treatment with dexamethasone.

The effect of dexamethasone therapy on fluid balance, lung function and requirement for respiratory support has been assessed. Ten premature infants were studied, they had a median gestational age of 28 weeks. None of the infants had any improvement in the respiratory status for 48 h prior to commencing dexamethasone. Fluid balance, pulmonary function and requirement for respiratory support were measured 12 h prior to and for 36 h after receiving dexamethasone. There were no significant changes in fluid input over the study period, but urine output increased significantly after 12 h of dexamethasone therapy (P < 0.02). Compliance of the respiratory system only significantly improved after 36 h of dexamethasone therapy (P < 0.03), this was associated with a significant change in the inspired oxygen concentration (P < 0.05). We conclude that the improvement in respiratory status resulting from dexamethasone therapy is preceded by a diuresis.

Dexamethasone↗
PubMed2004

The effects of dexamethasone and betamethasone on surfactant protein-B messenger RNA expression in human type II pneumocytes and human lung adenocarcinoma cells.

OBJECTIVE: The purpose of this study was to compare the effect of a single 48-hour exposure to betamethasone or dexamethasone in the NCI-H441 cell line and in human type II pneumocytes. STUDY DESIGN: NCI-H441 cells were exposed 48 hours to varying concentrations of betamethasone or dexamethasone (10(-10) to 10(-7) mol/L) alone or in combination with 1 mmol/L dibutyryl cyclic adenosine monophosphate. Likewise, human type II pneumocytes were exposed 48 hours to varying concentrations of betamethasone or dexamethasone (10(-9) to 10(-7) mol/L) alone or in combination with 1 mmol/L dibutyryl cyclic adenosine monophosphate. The measured outcome was the stimulatory effect on surfactant protein B gene transcription as expressed by surfactant protein B messenger RNA accumulation. The experiment was conducted 5 times in NCI-H441 cells and 6 times in type II cells, in parallel with control. Surfactant protein B messenger RNA was determined at control level and 48 hours after exposure by quantitative reverse transcription-polymerase chain reaction. RESULTS: A similar dose-dependent response in surfactant protein B messenger RNA expression was seen with both betamethasone and dexamethasone. In human type II pneumocytes, the inductive profile of surfactant protein B messenger RNA after 48-hour exposure to betamethasone or dexamethasone was similar to that seen in the NCI-H441 cells. CONCLUSION: Dexamethasone and betamethasone achieved similar dose-response patterns of surfactant protein-B expression in vitro.

Adenocarcinoma↗