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Four prenylflavonoids, kurarinone ( 1), a chalcone of 1, kuraridin ( 2), kurarinol ( 3), << kushenol H >> ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on diacylglycerol acyltransferase ([[ DGAT ]]).

Four prenylflavonoids, kurarinone ( 1), a chalcone of 1, kuraridin ( 2), kurarinol ( 3), kushenol H ( 4) and << kushenol K >> ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on [[ diacylglycerol acyltransferase ]] (DGAT).

Four prenylflavonoids, kurarinone ( 1), a chalcone of 1, kuraridin ( 2), kurarinol ( 3), kushenol H ( 4) and << kushenol K >> ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on diacylglycerol acyltransferase ([[ DGAT ]]).

Four prenylflavonoids, << kurarinone >> ( 1), a chalcone of 1, kuraridin ( 2), kurarinol ( 3), kushenol H ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on [[ diacylglycerol acyltransferase ]] (DGAT).

Four prenylflavonoids, << kurarinone >> ( 1), a chalcone of 1, kuraridin ( 2), kurarinol ( 3), kushenol H ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on diacylglycerol acyltransferase ([[ DGAT ]]).

Four prenylflavonoids, kurarinone ( 1), a << chalcone >> of 1, kuraridin ( 2), kurarinol ( 3), kushenol H ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on [[ diacylglycerol acyltransferase ]] (DGAT).

Four prenylflavonoids, kurarinone ( 1), a << chalcone >> of 1, kuraridin ( 2), kurarinol ( 3), kushenol H ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on diacylglycerol acyltransferase ([[ DGAT ]]).

Four << prenylflavonoids >>, kurarinone ( 1), a chalcone of 1, kuraridin ( 2), kurarinol ( 3), kushenol H ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on [[ diacylglycerol acyltransferase ]] (DGAT).

Four << prenylflavonoids >>, kurarinone ( 1), a chalcone of 1, kuraridin ( 2), kurarinol ( 3), kushenol H ( 4) and kushenol K ( 5) isolated from the roots of Sophora flavescens were investigated for their inhibitory effects on diacylglycerol acyltransferase ([[ DGAT ]]).

The << flavonoids >> inhibited [[ DGAT ]] activity in a dose-dependent manner with IC50 values of 10.9 microM ( 1), 9.8 microM ( 2), 8.6 microM ( 3), 142.0 microM ( 4) and 250 microM ( 5).

These data suggest that the << lavandulyl >> side chain and the position of the hydroxy group are important for high [[ DGAT ]] inhibitory activity.

These data suggest that the lavandulyl side chain and the position of the << hydroxy >> group are important for high [[ DGAT ]] inhibitory activity.

Dexamethasone (DXM) decreased the expression of CXCL-8, VEGF, and iNOS induced by reIL-4, while << 1400W dihydrochloride >> (1400W), a selective inhibitor of iNOS, decreased the expression of [[ E-selectin ]], VEGF, and iNOS.

Dexamethasone (DXM) decreased the expression of CXCL-8, VEGF, and iNOS induced by reIL-4, while << 1400W dihydrochloride >> (1400W), a selective inhibitor of iNOS, decreased the expression of E-selectin, [[ VEGF ]], and iNOS.

Dexamethasone (DXM) decreased the expression of CXCL-8, VEGF, and iNOS induced by reIL-4, while << 1400W dihydrochloride >> (1400W), a selective inhibitor of iNOS, decreased the expression of E-selectin, VEGF, and [[ iNOS ]].

Dexamethasone (DXM) decreased the expression of CXCL-8, VEGF, and iNOS induced by reIL-4, while 1400W dihydrochloride (<< 1400W >>), a selective inhibitor of iNOS, decreased the expression of [[ E-selectin ]], VEGF, and iNOS.

Dexamethasone (DXM) decreased the expression of CXCL-8, VEGF, and iNOS induced by reIL-4, while 1400W dihydrochloride (<< 1400W >>), a selective inhibitor of iNOS, decreased the expression of E-selectin, [[ VEGF ]], and iNOS.

Dexamethasone (DXM) decreased the expression of CXCL-8, VEGF, and iNOS induced by reIL-4, while 1400W dihydrochloride (<< 1400W >>), a selective inhibitor of iNOS, decreased the expression of E-selectin, VEGF, and [[ iNOS ]].

<< Dexamethasone >> (DXM) decreased the expression of [[ CXCL-8 ]], VEGF, and iNOS induced by reIL-4, while 1400W dihydrochloride (1400W), a selective inhibitor of iNOS, decreased the expression of E-selectin, VEGF, and iNOS.

<< Dexamethasone >> (DXM) decreased the expression of CXCL-8, [[ VEGF ]], and iNOS induced by reIL-4, while 1400W dihydrochloride (1400W), a selective inhibitor of iNOS, decreased the expression of E-selectin, VEGF, and iNOS.

<< Dexamethasone >> (DXM) decreased the expression of CXCL-8, VEGF, and [[ iNOS ]] induced by reIL-4, while 1400W dihydrochloride (1400W), a selective inhibitor of iNOS, decreased the expression of E-selectin, VEGF, and iNOS.

Dexamethasone (<< DXM >>) decreased the expression of [[ CXCL-8 ]], VEGF, and iNOS induced by reIL-4, while 1400W dihydrochloride (1400W), a selective inhibitor of iNOS, decreased the expression of E-selectin, VEGF, and iNOS.

Dexamethasone (<< DXM >>) decreased the expression of CXCL-8, [[ VEGF ]], and iNOS induced by reIL-4, while 1400W dihydrochloride (1400W), a selective inhibitor of iNOS, decreased the expression of E-selectin, VEGF, and iNOS.

Dexamethasone (<< DXM >>) decreased the expression of CXCL-8, VEGF, and [[ iNOS ]] induced by reIL-4, while 1400W dihydrochloride (1400W), a selective inhibitor of iNOS, decreased the expression of E-selectin, VEGF, and iNOS.

Dexamethasone (DXM) decreased the expression of CXCL-8, VEGF, and iNOS induced by reIL-4, while << 1400W dihydrochloride >> (1400W), a selective inhibitor of [[ iNOS ]], decreased the expression of E-selectin, VEGF, and iNOS.

Dexamethasone (DXM) decreased the expression of CXCL-8, VEGF, and iNOS induced by reIL-4, while 1400W dihydrochloride (<< 1400W >>), a selective inhibitor of [[ iNOS ]], decreased the expression of E-selectin, VEGF, and iNOS.

<< DXM >> and 1400W attenuated the mRNA expression of [[ E-selectin ]] and iNOS induced by the costimulation of reIL-4, reTNF-alpha, and LPS.

<< DXM >> and 1400W attenuated the mRNA expression of E-selectin and [[ iNOS ]] induced by the costimulation of reIL-4, reTNF-alpha, and LPS.

DXM and << 1400W >> attenuated the mRNA expression of [[ E-selectin ]] and iNOS induced by the costimulation of reIL-4, reTNF-alpha, and LPS.

DXM and << 1400W >> attenuated the mRNA expression of E-selectin and [[ iNOS ]] induced by the costimulation of reIL-4, reTNF-alpha, and LPS.

The beneficial role of << 17beta-estradiol >> on blood pressure, cardiac hypertrophy, vascular [[ osteopontin ]] expression, perivascular fibrosis, and impaired NO-dependent relaxation of isolated aortic rings was completely abrogated by coadministration of medroxyprogesterone acetate.

The beneficial role of 17beta-estradiol on blood pressure, cardiac hypertrophy, vascular << osteopontin >> expression, perivascular fibrosis, and impaired NO-dependent relaxation of isolated aortic rings was completely abrogated by coadministration of [[ medroxyprogesterone acetate ]].

At a low pH (pH 7.4), but not pH 7.9, << ifenprodil >> reduces the mean open time of [[ GluN1 ]]/GluN2B receptors, which may be responsible for its usefulness as a context-dependent inhibitor in conditions like ischemia and stroke, when the pH of the extracellular milieu becomes acidic.

At a low pH (pH 7.4), but not pH 7.9, << ifenprodil >> reduces the mean open time of GluN1/[[ GluN2B ]] receptors, which may be responsible for its usefulness as a context-dependent inhibitor in conditions like ischemia and stroke, when the pH of the extracellular milieu becomes acidic.

Pharmacological doses of the << mTOR >> inhibitor [[ rapamycin ]] reduce albuminura in diabetes.

High << glucose >> (HG) induces apoptosis of podocytes, inhibits AMPK activation, inactivates tuberin and activates [[ mTOR ]].

High << glucose >> (HG) induces apoptosis of podocytes, inhibits AMPK activation, inactivates [[ tuberin ]] and activates mTOR.

High << glucose >> (HG) induces apoptosis of podocytes, inhibits [[ AMPK ]] activation, inactivates tuberin and activates mTOR.

Inhibition of mTOR by low dose << rapamycin >> decreases HG-induced [[ Nox4 ]] and Nox1, NADPH oxidase activity and podocyte apoptosis.

Inhibition of mTOR by low dose << rapamycin >> decreases HG-induced Nox4 and [[ Nox1 ]], NADPH oxidase activity and podocyte apoptosis.

Inhibition of << mTOR >> by low dose [[ rapamycin ]] decreases HG-induced Nox4 and Nox1, NADPH oxidase activity and podocyte apoptosis.

Inhibition of mTOR by low dose << rapamycin >> decreases HG-induced Nox4 and Nox1, [[ NADPH oxidase ]] activity and podocyte apoptosis.

Inhibition of << mTOR >> by small dose of [[ rapamycin ]] reduces podocyte apoptosis, attenuates glomerular injury and albuminuria.

Systemic administration of << beta2-adrenoceptor >> agonists, [[ formoterol ]] and salmeterol, elicit skeletal muscle hypertrophy in rats at micromolar doses.

Systemic administration of << beta2-adrenoceptor >> agonists, formoterol and [[ salmeterol ]], elicit skeletal muscle hypertrophy in rats at micromolar doses.

Two beta(2)-agonists, << formoterol >> and salmeterol, are approved for treating asthma and have an extended duration of action and increased safety, associated with greater [[ beta(2)-adrenoceptor ]] selectivity.

Two beta(2)-agonists, formoterol and << salmeterol >>, are approved for treating asthma and have an extended duration of action and increased safety, associated with greater [[ beta(2)-adrenoceptor ]] selectivity.

A dose of 25 microg kg(-1) day(-1) of << formoterol >> elicited greater EDL and soleus hypertrophy than salmeterol, but resulted in similar [[ beta-adrenoceptor ]] downregulation.

A dose of 25 microg kg(-1) day(-1) of formoterol elicited greater EDL and soleus hypertrophy than << salmeterol >>, but resulted in similar [[ beta-adrenoceptor ]] downregulation.

Clinical utility of << acarbose >>, an [[ alpha-glucosidase ]] inhibitor in cardiometabolic disorders.

<< Acarbose >>, an [[ alpha-glucosidase ]] inhibitor, delays the absorption of carbohydrate from the small intestine, thereby reducing postprandial hyperglycemia.

The values of mean corpuscular hemoglobin concentration and mean corpuscular << hemoglobin >> increased in the [[ STX ]] group.

The values of mean corpuscular << hemoglobin >> concentration and mean corpuscular hemoglobin increased in the [[ STX ]] group.

First, we showed that intracerebroventricular administration of << glucose >> in rats increases [[ DBI ]] expression in hypothalamic glial-like tanycytes.

On phosphorylation of << Ser40 >> by [[ protein kinase A ]], the affinity for H4biopterin increased ([S]0.5 = 11 +/- 2 microM) and the negative cooperativity was amplified (h = 0.27 +/- 0.03).

Disposition of a specific << cyclooxygenase-2 >> inhibitor, [[ valdecoxib ]], in human.

<< Valdecoxib >> is a potent and specific inhibitor of [[ cyclooxygenase-2 ]], which is used for the treatment of rheumatoid arthritis, osteoarthritis, and the dysmenorrhea pain.

In mechanistic studies, << Silibinin >> decreased the protein level of [[ p34cdc2 ]], which might be the possible molecular mechanism of Silibinin efficacy on the growth inhibition in SGC-7901 cells.

In addition, << Silibinin >> caused an increase in [[ p53 ]] and p21 protein level as well as mRNA levels.

In addition, << Silibinin >> caused an increase in p53 and [[ p21 ]] protein level as well as mRNA levels.

4-Hydroxynonenal (<< 4-HNE >>) is a mutagenic alpha,beta-unsaturated aldehyde produced during oxidative injury that is conjugated by several [[ glutathione S-transferase ]] (GST) isoforms.

4-Hydroxynonenal (<< 4-HNE >>) is a mutagenic alpha,beta-unsaturated aldehyde produced during oxidative injury that is conjugated by several glutathione S-transferase ([[ GST ]]) isoforms.

<< 4-Hydroxynonenal >> (4-HNE) is a mutagenic alpha,beta-unsaturated aldehyde produced during oxidative injury that is conjugated by several [[ glutathione S-transferase ]] (GST) isoforms.

<< 4-Hydroxynonenal >> (4-HNE) is a mutagenic alpha,beta-unsaturated aldehyde produced during oxidative injury that is conjugated by several glutathione S-transferase ([[ GST ]]) isoforms.

4-Hydroxynonenal (4-HNE) is a mutagenic << alpha,beta-unsaturated aldehyde >> produced during oxidative injury that is conjugated by several [[ glutathione S-transferase ]] (GST) isoforms.

4-Hydroxynonenal (4-HNE) is a mutagenic << alpha,beta-unsaturated aldehyde >> produced during oxidative injury that is conjugated by several glutathione S-transferase ([[ GST ]]) isoforms.

The alpha class << human GSTA4-4 >> enzyme (hGSTA4-4) has a particularly high catalytic efficiency toward [[ 4-HNE ]] conjugation.

The alpha class human GSTA4-4 enzyme (<< hGSTA4-4 >>) has a particularly high catalytic efficiency toward [[ 4-HNE ]] conjugation.

HepG2 cells transfected with an hGSTA4 vector construct exhibited high steady-state hGSTA4 mRNA, high << GST-4 >>[[ 4-HNE ]] catalytic activities, but lower basal glutathione (GSH) concentrations relative to insert-free vector (control) cells.

Specifically, << hGSTA4 >> cells had significantly higher GSH concentrations when exposed to 5-15 microM [[ 4-HNE ]], but not at 20 microM 4-HNE, suggesting extensive GSH utilization at high concentrations of 4-HNE.

Specifically, << hGSTA4 >> cells had significantly higher GSH concentrations when exposed to 5-15 microM 4-HNE, but not at 20 microM [[ 4-HNE ]], suggesting extensive GSH utilization at high concentrations of 4-HNE.

In summary, our data indicates that over-expression of hGSTA4 at levels conferring high << GST >>-[[ 4-HNE ]] conjugating activity confers a partial growth advantage to HepG2 cells and protects against 4-HNE oxidative injury.

However, the loss of proliferative capacity of << hGSTA4 >> cells challenged with levels of [[ 4-HNE ]] associated with severe oxidative stress indicates a role of other aldehyde metabolizing enzymes, and/or GSH-electrophile transporter proteins, in providing full cellular protection against 4-HNE toxicity.

OBJECTIVE: Preclinical evaluation of << DRF 2655 >>, a peroxisome proliferator-activated receptor alpha (PPARalpha) and [[ PPARgamma ]] agonist, as a body-weight lowering, hypolipidemic and euglycemic agent.

OBJECTIVE: Preclinical evaluation of << DRF 2655 >>, a [[ peroxisome proliferator-activated receptor alpha ]] (PPARalpha) and PPARgamma agonist, as a body-weight lowering, hypolipidemic and euglycemic agent.

OBJECTIVE: Preclinical evaluation of << DRF 2655 >>, a peroxisome proliferator-activated receptor alpha ([[ PPARalpha ]]) and PPARgamma agonist, as a body-weight lowering, hypolipidemic and euglycemic agent.

RESULTS: << DRF 2655 >> showed concentration-dependent transactivation of [[ PPARalpha ]] and PPARgamma.

RESULTS: << DRF 2655 >> showed concentration-dependent transactivation of PPARalpha and [[ PPARgamma ]].

db/db mice treated with << DRF 2655 >> showed 5- and 3.6-fold inhibition in phosphoenolpyruvate carboxykinase and glucose 6-phosphatase activity and 651% and 77% increases in the beta-oxidation enzymes [[ carnitine palmitoyltransferase ]] and carnitine acetyltransferase, respectively.

db/db mice treated with << DRF 2655 >> showed 5- and 3.6-fold inhibition in phosphoenolpyruvate carboxykinase and glucose 6-phosphatase activity and 651% and 77% increases in the beta-oxidation enzymes carnitine palmitoyltransferase and [[ carnitine acetyltransferase ]], respectively.

db/db mice treated with << DRF 2655 >> showed 5- and 3.6-fold inhibition in [[ phosphoenolpyruvate carboxykinase ]] and glucose 6-phosphatase activity and 651% and 77% increases in the beta-oxidation enzymes carnitine palmitoyltransferase and carnitine acetyltransferase, respectively.

db/db mice treated with << DRF 2655 >> showed 5- and 3.6-fold inhibition in phosphoenolpyruvate carboxykinase and [[ glucose 6-phosphatase ]] activity and 651% and 77% increases in the beta-oxidation enzymes carnitine palmitoyltransferase and carnitine acetyltransferase, respectively.

The enzyme << cyclo-oxygenase >> catalyses the oxygenation of arachidonic acid, leading to the formation of [[ prostaglandins ]].

The enzyme << cyclo-oxygenase >> catalyses the oxygenation of [[ arachidonic acid ]], leading to the formation of prostaglandins.

<< hCOX-1 >> had a specific activity of 18.8 mumol of O2/mg with a Km of 13.8 microM for [[ arachidonate ]] and Vmax. of 1500 nmol of O2/nmol of enzyme, whereas hCOX-2 had a specific activity of 12.2 mumol of O2/mg with a Km of 8.7 microM for arachidonate and a Vmax. of 1090 nmol of O2/nmol of enzyme.

hCOX-1 had a specific activity of 18.8 mumol of O2/mg with a Km of 13.8 microM for arachidonate and Vmax. of 1500 nmol of O2/nmol of enzyme, whereas << hCOX-2 >> had a specific activity of 12.2 mumol of O2/mg with a Km of 8.7 microM for [[ arachidonate ]] and a Vmax. of 1090 nmol of O2/nmol of enzyme.

<< Indomethacin >> inhibited both [[ hCOX-1 ]] and hCOX-2, whereas NS-398 and Dup-697 selectively inhibited hCOX-2.

<< Indomethacin >> inhibited both hCOX-1 and [[ hCOX-2 ]], whereas NS-398 and Dup-697 selectively inhibited hCOX-2.

Indomethacin inhibited both hCOX-1 and hCOX-2, whereas << NS-398 >> and Dup-697 selectively inhibited [[ hCOX-2 ]].

Indomethacin inhibited both hCOX-1 and hCOX-2, whereas NS-398 and << Dup-697 >> selectively inhibited [[ hCOX-2 ]].

Both << NS-398 >> and Dup-697 exhibited time-dependent inactivation of [[ hCOX-2 ]], as did indomethacin on both enzymes.

Both NS-398 and << Dup-697 >> exhibited time-dependent inactivation of [[ hCOX-2 ]], as did indomethacin on both enzymes.

Both NS-398 and Dup-697 exhibited time-dependent inactivation of << hCOX-2 >>, as did [[ indomethacin ]] on both enzymes.

The competitive inhibitor of << hCOX-1 >>, [[ mefenamic acid ]], also displayed competitive inhibition of hCOX-2.

The competitive inhibitor of hCOX-1, << mefenamic acid >>, also displayed competitive inhibition of [[ hCOX-2 ]].

<< Doxycycline >> was shown to decrease cerebral [[ MMP-9 ]] activities and angiogenesis induced by vascular endothelial growth factor (VEGF).

<< Doxycycline >> was shown to decrease cerebral MMP-9 activities and angiogenesis induced by [[ vascular endothelial growth factor ]] (VEGF).

<< Doxycycline >> was shown to decrease cerebral MMP-9 activities and angiogenesis induced by vascular endothelial growth factor ([[ VEGF ]]).

Our results have shown that << MMP-9 >> messenger ribonucleic acid (mRNA) expression was inhibited by [[ doxycycline ]] starting at 10 mg/kg/day (P<0.02).

<< Minocycline >> showed more potent inhibition on [[ MMP-9 ]] mRNA expression, starting at 1 (P<0.005) and further at more than 30 (P<0.001) mg/kg/day.