Biomedical subjects

D H Kuo

Publications and source records attributed to D H Kuo.

5 recordsLinked to original sources

PubMed2001

Stimulatory effect of phenylephrine on the secretion of beta-endorphin from rat adrenal medulla in vitro.

In an attempt to investigate the role of alpha1-adrenoceptors in the regulation of opioid secretion from adrenal gland, phenylephrine was employed to investigate the effect on secretion of beta-endorphin-like immunoreactivity (BER) from adrenal medulla of rat in vitro. Phenylephrine enhanced the BER from isolated adrenal medulla in a concentration-dependent manner and this action was abolished by the antagonists of alpha1-adrenoceptors, prazosin and tamsulosin. Investigations of signal pathway further support that an activation of alpha1-adrenoceptors is responsible for the stimulatory effect of phenylephrine on BER secretion from adrenal medulla. In the presence of U73312, the specific inhibitor of phospholipase C (PLC), phenylephrine-induced change of BER was reduced in a concentration-dependent manner but it was not affected by U73343, the negative control of U73312. Moreover, chelerythrine and GF 109203X diminished the action of phenylephrine at concentration sufficient to inhibit protein kinase C (PKC). In conclusion, our results suggest that an activation of alpha1-adrenoceptors in adrenal medulla by phenylephrine may enhance the secretion of opioids from adrenal gland of rat via signals of PLC-PKC pathway.

Adrenal Medulla↗

PubMed2000

Structure-activity relationships of anthraquinones in the decrease of intestinal motility.

The effects of substituted anthraquinones on intestinal motility were evaluated in-vitro using rabbit small intestinal strips. This structure-activity relationship study revealed the critical requirement of a hydroxy group at R2 position. The intestinal motility was inhibited 50% (IC50) by emodine (8 microM), 2-hydroxy anthraquinone (20 microM), 2,6-dihydroxy anthraquinone (25 microM), 2,7-dihydroxy anthraquinone (10 microM), 1,2,4-trihydroxy anthraquinone (80 microM) and 1,2,5,8-tetra-hydroxyanthraquinone (9 microM). The presence of other polar groups at R2 position such as an amino, aldehyde and carboxylic acid group significantly reduced the activity (IC50 360-400 microM). The presence of a methyl group and esterification of the carboxylic acid at R2 position was found to abolish the activity. These data are useful for the future development of anthraquinones as laxative agents.

Animals↗

PubMed1999

Investigations of the mechanism of the reduction of plasma glucose by cold-stress in streptozotocin-induced diabetic rats.

Exposure to a cold environment may increase the activity of the sympathetic nervous system inducing an elevation of plasma norepinephrine and may result in hyperglycemia. In the present study, we found that a hypoglycemic effect was produced in streptozotocin-induced diabetic rats after cold-exposure at 4 degrees C for 1 h. In addition to the blockade of this hypoglycemic effect by guanethidine (a ganglion-blocking agent) and prazosin (an alpha1-adrenoceptor antagonist), an increase of plasma norepinephrine was also observed in streptozotocin-induced diabetic rats receiving this cold-stress. Participation of sympathetic hyperactivity can thus be considered. Furthermore, naloxone, in a dose (0.5 mg/kg, i.p.) sufficient to block opioid receptors, reversed this hypoglycemia. Also, an increase of plasma beta-endorphin-like immunoreactivity was observed in streptozotocin-induced diabetic rats receiving this cold-stress. Intravenous injection of beta-endorphin into streptozotocin-induced diabetic rats produced a lowering of plasma glucose. Administration of methoxamine at a dose sufficient to activate the alpha1-adrenoceptors produced hypoglycemia and a similar increase of plasma beta-endorphin-like immunoreactivity in streptozotocin-induced diabetic rats. However, plasma beta-endorphin-like immunoreactivity level was not modified by similar treatment with methoxamine or cold-stress in normoglycemic rats. Therefore, beta-endorphin appears to be responsible for the induction of hypoglycemic effects in streptozotocin-induced diabetic rats after cold exposure which is different to the response in normal rats.

Animals↗

PubMed1998

Modification of superoxide dismutase (SOD) mRNA and activity by a transient hypoxic stress in cultured glial cells.

In order to understand the role of superoxide dismutase (SOD) in response to transient hypoxia or hypoxia-reperfusion in astrocytes, the present study performed an in vitro investigation using rat glial cells in culture. Hypoxia was induced by an incubation with nitrogen gas for 10 min and that followed a further reperfusion with air for 10 min was indicating as hypoxia-normoxia. Activity of SOD was determined by the reduction of nitroblue tetrazolium (NTB). Changes of mRNA for Cu,Zn-SOD or Mn-SOD were also characterized using Northern blotting analysis. Transient hypoxia increased the activity of Mn-SOD but not that of Cu,Zn-SOD in glial cells. Expression of mRNA for SOD was also elevated in cells received hypoxia and the mRNA level for Mn-SOD raised higher than that for Cu,Zn-SOD. In cells received hypoxia-reperfusion, these changes of SOD both the activity and the mRNA level were not observed. Otherwise, the SOD protein amount, both Cu,Zn-SOD and Mn-SOD, identified by Western blotting was not changed in glial cells receiving hypoxic stress or not. The obtained results suggest that gene expression and activity of Mn-SOD in glial cells can be activated in response to the transient hypoxic stress.

Animals↗

PubMedDate not supplied

Synthesis and vasorelaxing evaluation of alpha-methylidene-gamma-butyrolactone bearing quinolin-2(1H)-one and 3,4-dihydroquinolin-2(1H)-one derivatives.

The main objective of this investigation was to explore the vasorelaxing structure-activity relationships of alpha-methylidene-gamma-butyrolactone bearing quinolin-2(1H)-ones and their 3,4-dihydro derivatives. These target compounds were synthesised in two steps starting from aryl-OH which was treated with a bromomethyl ketone followed by a Reformatsky-type condensation. Quinolin-2(1H)-one alpha-methylidene-gamma-butyrolactones exhibited less vasorelaxing activity than their 3,4-dihydro counterparts. Compounds with a methyl or a phenyl group at the C(gamma) of the lactone were more vasorelaxant than the C(gamma)-fluorophenyl derivatives in the 3,4-dihydroquinolin-2(1H)-one series. When comparing the positional isomers, alpha-methylidene-gamma-butyrolactone substituted at the 7-position of the 3,4-dihydroquinolin-2(1H)-ones were more active than their 6-substituted counterparts, which in turn were more active than the 8-substituted derivatives. The vasorelaxing effect of these 3,4-dihydroquinolin-2(1H)-ones was proved to be dose dependent. Among them, 7-[(2,3,4,5-tetrahydro-4-methylidene-5-oxo-2-phenyfuran-2-yl)methoxy]-quinolin-2(1H)-one (10b) was the most potent with an IC(50) of 9.2 microM on the KCl-induced vasoconstriction of pig coronary arteries.

4-Butyrolactone↗