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Biomedical subjects

M H Malone

Publications and source records attributed to M H Malone.

At least 19 recordsLinked to original sources

Thioredoxin-interacting protein (txnip) is a glucocorticoid-regulated primary response gene involved in mediating glucocorticoid-induced apoptosis.

Glucocorticoid hormones induce apoptosis in lymphoid cells. This process is transcriptionally regulated and requires de novo RNA/protein synthesis. However, the full spectrum of glucocorticoid-regulated genes mediating this cell death process is unknown. Through gene expression profiling we discovered that the expression of thioredoxin-intereacting protein (txnip) mRNA is significantly induced by the glucocorticoid hormone dexamethasone not only in the murine T-cell lymphoma line WEHI7.2, but also in normal mouse thymocytes. This result was confirmed by Northern blot analysis in multiple models of dexamethasone-induced apoptosis. The induction of txnip mRNA by dexamethasone appears to be mediated through the glucocorticoid receptor as it is blocked in the presence of RU486, a glucocorticoid receptor antagonist. Deletion and mutation analysis of the txnip promoter identified a functional glucocorticoid response element in the txnip promoter. Reporter assays demonstrated that this glucocorticoid response element was necessary and sufficient for induction of txnip by dexamethasone. Expression of a GFP-TXNIP fusion protein was sufficient to induce apoptosis in WEHI7.2 cells, and repression of endogenous txnip by RNA interference inhibited dexamethasone-induced apoptosis in WEHI7.2 cells. Together, these findings indicate that txnip is a novel glucocorticoid-induced primary target gene involved in mediating glucocorticoid-induced apoptosis.

Anti-Inflammatory Agents↗

Effect of various pretreatments on the hypothermic activity of repin in naive rats.

Repin is a sesquiterpene lactone found in Centaurea solstitialis, a plant responsible for Parkinson-like disease in horses. Repin, on intraperitoneal (i.p.) injection, produces a dose-dependent and highly significant hypothermia in naive rats. The hypothermia is long-lasting with a peak 3 h after the injection and a return to normal temperature after more than 8 h. The effects of atropine sulfate, atropine methylbromide, propranolol, metergoline, ketanserin, diphenhydramine and apomorphine pretreatment on repin-induced hypothermia were investigated. None of the pretreatments directly antagonized repin's hypothermic effect. However, partial but significant reversals of hypothermia by atropine sulfate, metergoline, ketanserin, diphenhydramine and apomorphine were observed 2-4 h after the repin injection. These late-onset effects are probably due to secondary physiological mechanisms. On the other hand, propranolol, at 20 mg/kg i.p., clearly accentuated both the early-onset (30-90 min) and late-onset (2-4 h) hypothermic effects of repin.

Animals↗

Inhibitory effect of 5-hydroxytryptamine on rat stomach fundus: mediated indirectly by activation of noradrenaline release.

Biphasic cumulative concentration-response curves to 5-hydroxytryptamine (5-HT) and alpha-methyl-5-hydroxytryptamine (alpha-Me-5-HT) using rat stomach fundus in the presence of 50 microM pargyline suggested two sites of interaction (high and low affinity). The order of agonist potencies of 5-HT agonists for the high-affinity (contractile) response confirmed reports of a strong correlation of the 5-HT2B (contractile) receptor on fundus with reported rat brain (radioligand binding) pKd values at the 5-HT2C receptor (r = 0.94, b = 0.93 P < 0.01). 1(1-Naphthyl)-piperazine and ketanserin antagonized the high-affinity responses. The order of potencies for the low affinity (inhibitory) response was: alpha-Me-5-HT > 5-HT. Preincubation with mianserin or S-(-)propranolol, pretreatment with reserpine and removal of the mucosa layer resulted in amplification of the contractile effects and disappearance or reversal of the inhibitory effects of 5-HT. Activation of a second receptor site inducing catecholamine release may explain this effect of 5-HT on rat stomach fundus.

Animals↗

Heimia salicifolia: a phytochemical and phytopharmacologic review.

Heimia salicifolia grows wild from Mexico to Argentina. The aerial parts have a wide folk reputation for antisyphilitic, sudorific, antipyretic, laxative and diuretic activity, and are reported to be useful in preparing post partum baths and to enhance wound healing. Its four most studied alkaloids are vertine, lyfoline, lythrine and nesodine. Structural relationships of the Heimia alkaloids and certain synthetic 4-arylquinolizidines are reviewed here. Preliminary clinical evaluation indicates that vertine and lythrine given orally appear to lack the psychodysleptic activity that has been touted for native brews said to incorporate H. salicifolia. Most of the animal studies discussed here have focused on the ataractic, antiinflammatory and antispasmodic potential of vertine and on the hydrodiuretic potential of lythrine and decine, a structurally related alkaloid found in Decodon verticillatus. The ataractic activity of vertine does not appear to be dependent on the depletion or blockade of catecholamines, while its antiinflammatory capacity seen in both exudative and immunologic systems seems to be dependent in part on an intact pituitary-adrenal system and in part on inhibition of prostaglandin synthase. The antisplasmodic activity of vertine has been demonstrated on many isolated tissues using different agonists, but appears to be largely musculotropic in nature. Only lythrine and decinine have been shown to be true hydrodiuretics and may prove to be useful in treating Addison's disease and general nephrosis. A number of synthetic 4-arylquinolizidines and related compounds appear to possess antiinflammatory potential.

Animals↗

Pharmacological and chemical screening of Byrsonima crassifolia, a medicinal tree from Mexico. Part I.

Leaf and bark extracts of Byrsonima crassifolia displayed concentration-dependent, spasmogenic effects on rat fundus in vitro and biphasic effects on rat jejunum and ileum in vitro. Dose-related in vivo effects in intact rats using hippocratic screening were: decrease in motor activity, mild analgesia, back tonus, enophthalmos, reversible palpebral ptosis, ear blanching, Robichaud positive, catalepsy (awake) and strong hypothermia. Rat fundus in vitro was used as the bioassay to carry out an activity-directed separation. Bioactive material was concentrated in a 2% acetic acid leaf extract (HOAcE). Potency of HOAcE was increased by the presence of pargyline in the bathing solution. HOAcE was antagonized noncompetively by 1(1-naphthyl) piperazine (1-NP) and cyproheptadine and antagonized competitively by atropine (ATR). Cumulative concentration-response curves of HOAcE and serotonin (5-HT) did not show significant departure from parallelism (P > 0.1) and 5-HT potency was 6040 times that of HOAcE (95% confidence limits: 4620-7850). Solvent extraction of HOAcE split the spasmogenic activity of HOAcE into two types: (i) high-efficacy, low-potency, n-butanol-extracted, pargyline- and 1-NP-sensitive, ATR-insensitive activity, and (ii) low-efficacy, high-potency, ethyl acetate-extracted, pargyline-insensitive, ATR- and 1-NP-sensitive activity. HOAcE lacked muscarinic and nicotinic effects on rat jejunum and frog rectus abdominis. Results suggest the presence of more than one spasmogenic compound in the plant.

Animals↗

Testing for circadian differences in lethality for intravenous ouabain in male mice.

Using a randomized, balanced design and double-blind methodology, ouabain octahydrate was administered intravenously to male mice at six clock times. Eight runs were conducted using six constant dosage levels. All the dose-response curves at the clock times of 02:30, 06:30, 10:30, 14:30, 18:30 and 22:30 were parallel and no significant differences were noted between the respective LD50 determinations using nomograph methods. Independent chi-square analysis of all lethality data indicated no significant variation in response between clock times and between runs but a very highly significant difference between doses. Using regression methods, onset time for death was shown to vary inversely with log-dosage, but those periods of possible increased susceptibility could not be correlated with a shortened time to death. These findings are consistent with a random variation in lethality in regard to clock time rather than a true circadian pattern. The pooled (N = 576) intravenous LD50 for ouabain octahydrate was 3.75 mg/kg with 95% confidence limits of 3.60-3.90 mg/kg or, when calculated as anhydrous ouabain, 3.01 (2.89-3.13) mg/kg.

Animals↗

Effect of chronic cocaine administration and cocaine withdrawal on coronary flow rate and heart rate responses to epinephrine and cocaine in isolated perfused rat hearts.

The acute dose-dependent effects of epinephrine and cocaine on heart rate and coronary flow rate (CFR) were examined in isolated, perfused (Langendorff) rat hearts from animals: i) pretreated with daily cocaine injections (20 mg/kg/day) for 8 weeks; ii) after 2-day withdrawal from 8-week cocaine pretreatment; iii) vehicle-treated controls. Chronic cocaine (CC) hearts were significantly less sensitive to the chronotropic effects of epinephrine than control (C) or withdrawal (CW) hearts. CW hearts exhibited significantly higher heart rates in response to epinephrine than C and CC hearts. Epinephrine alone (2.5 x 10(-7) M) decreased CFR 11% (C), 9%(CC), 14%(CW) from respective baseline levels. Cocaine alone had no significant effect on CFR in C hearts but produced slight dose-dependent decrements in CFR in CC and particularly CW hearts at higher doses. Cocaine plus epinephrine markedly decreased CFR in all groups, particularly in CW hearts. The results indicate that chronic daily cocaine administration produces a functional tolerance of the heart to the chronotropic actions of epinephrine but a 2-day withdrawal from chronic cocaine results in a rebound supersensitivity to adrenergic stimulation and cocaine's sympathomimetic effects. In addition, cocaine produces only minor decrements in coronary flow in the rat heart, while cocaine acts synergisticallly with epinephrine to produce a marked decrease in CFR.

Animals↗

Prostaglandin synthetase inhibition by alkaloids of Heimia salicifolia.

Two alkaloids from Heimia salicifolia, cryogenine and nesodine, were respectively 2.48 and 2.24 times as potent as aspirin as inhibitors of prostaglandin synthetase prepared from bovine seminal vesicles. Reference compounds, indomethacin and phenylbutazone, were respectively 2800 and 8.75 times as potent while a synthetic analogue of cryogenine, JB-1-0, was 0.656 times the potency of aspirin. This activity may help to explain the traditional medicine use of H. salicifolia in the Americas.

Alkaloids↗

Opioid receptor effects of two 3-amino-2,2-dimethyltetralin analogs in guinea pig ileum longitudinal muscle.

Two substituted analogs of 3-amino-2,2-dimethyltetralin, namely 3-dimethylamino-2,2-dimethyl-7-hydroxy-1-tetralone HBr (J) and 3-dimethylamino-2,2-dimethyl-7-hydroxy-1-tetralol (MRSAL), were evaluated for opioid agonist and antagonist activity using the electrically driven guinea pig ileum longitudinal muscle preparation (GPI). Compound J appeared to be an opioid agonist with a preference for mu receptors while MRSAL was an opioid antagonist with little selectivity for mu or kappa receptors.

Animals↗

Pipradrol-induced hyperthermia in the rabbit.

Intravenous administration of the stimulant drug pipradrol evoked a dose-dependent hyperthermic response in rabbits. This drug effect was significantly reduced by pretreatment with chlorpromazine, phenoxybenzamine, intravenous BE-2254 or intracerebroventricular BE-2254. In animals pretreated with cyproheptadine or atropine, the hyperthermic effect was significantly potentiated. However, haloperidol, pimozide, diphenhydramine and pentobarbital failed to appreciably influence the drug response. These findings suggest that pipradrol-induced hyperthermia in the rabbit involves activation of central alpha-adrenergic receptors and is apparently enhanced by blockade of serotonergic or cholinergic receptors.

Animals↗

Differential effects of 5-hydroxytryptaminergic antagonists upon apomorphine- and lergotrile-induced hypothermia and stereotyped behaviour in rats.

The dopaminergic stimulants apomorphine and lergotrile both evoked hypothermia and stereotyped behaviour in rats. These drug effects were sensitive to antagonism by haloperidol, a dopaminergic receptor blocker. In rats pretreated with 5-hydroxytryptaminergic receptor blockers, cinanserin reduced apomorphine-induced hypothermia but cyproheptadine did not. Both cinanserin and cyproheptadine significantly potentiated lergotrile-induced hypothermia. Similarly, the stereotypic effects of apomorphine were partly reduced by cyproheptadine, although higher doses of cyproheptadine did potentiate lergotrile-induced stereotyped behaviour. These findings of different influences of 5-HT antagonists upon the effects of apomorphine and lergotrile indicate that these two dopaminergic stimulants may not work in identical manner to produce outwardly similar drug effects.

5-Hydroxytryptophan↗