• 약학회지
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• 제32권6호
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• pp.428-434
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• 1988

The effects of calcium and calcium antagonist, nifedipine on the adrenergic receptor-stimulated glycogenolysis were investigated in isolated rat hepatocytes. The hepatic glycogenolysis induced by alpha-adrenergic receptor stimulation depended on calcium ions, and beta-adrenergic activation was unrelated to calcium ions. Nifedipine decreased the alpha-adrenergic agonist-induced glucose release significantly and the decrease was depended on calcium ions. The glucose release induced by beta-adrenergic agonist was not inhibited by nifedipine.

• 대한수의학회지
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• 제43권4호
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• pp.563-571
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• 2003

Dysfunction of mesangial cells has been contributed to the onset of diabetic nephropathy. Insulin like growth factors (IGFs) are also implicated in the pathogenesis of diabetic nephropathy. However, it is not yet known about the effect of high glucose on IGF-I and IGF-II secretion in the mesangial cells. Furthermore, the relationship between cAMP and high glucose on the secretion of IGFs was not elucidated. Thus, we examined the mechanisms by which high glucose regulates secretion of IGFs in mesangial cells. Glucose increased IGF-I secretion in a time- (>8 hr) and dose- (>15 mM) dependent manner (p<0.05). Stimulatory effect of high glucose on IGF-I secretion is predominantly observed in 25 mM glucose (high glucose), while 25 mM glucose did not affect cell viability and lactate dehydrogenase release. High glucose also increased IGF-II secretion. The increase of IGF-I and IGF-II secretion is not mediated by osmotic effect, since mannitol and L-glucose did not affect IGF-I and IGF-II secretion. 8-Br-cAMP mimicked high glucose-induced secretion of IGF-I and IGF-II. High glucose-induced stimulation of IGF-I and IGF-II secretion was blocked not by pertussis toxin but by SQ 22536 (adenylate cyclase inhibitor). Rp-cAMP (cAMP antagonist), and myristoylated protein kinase A (PKA) inhibitor amide 14-22 (protein kinase A inhibitor). These results suggest that cAMP/PKA pathways independent of Gi protein may mediate high glucose-induced increase of IGF-I and IGF-II secretion in mesangial cells. Indeed, glucose (>15 mM glucose) increased cAMP formation. In conclusion, high glucose stimulates IGF-I and IGF-II secretion via cAMP/PKA pathway in mesangial cells.

• 공업화학
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• 제8권5호
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• pp.715-721
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• 1997

$W_1/O/W_2$ 다중유화의 내부수상($W_1$)에 전해질인 $MgSO_4$를 모델약물로 주입하여 안정성과 약물방출 거동을 현미경관찰, 점도 및 전도도의 변화를 통해 관찰하였다. 내상에 약물을 도입함으로써 내부와 외부수상간의 삼투압차를 유발하여 다중유화계의 불안정성을 초래하였으며 이를 완화하기 위하여 외부수상($W_2$)에 글루코즈를 첨가하여 효과를 살펴본 결과 글루코즈의 유효삼투압 당량이 내부에 포함된 약물의 삼투압 당량과 유사해짐에 따라 안정성이 향상되었을 뿐아니라 초기 약물방출 속도도 글루코즈 농도에 의해 조절할 수 있음을 발견하였다. 이는 삼투압차에 의한 수분 이동시 친수성 계면활성제를 동반하여 내부수상/오일상 계면을 파괴하는 것을 방지하기 때문으로 보인다. 또한 이와같은 현상은 오일상이 cetostearyl alcohol에 의하여 친수화되었을 때 뚜렷하게 나타났다.

• 대한수의학회지
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• 제49권1호
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• pp.9-15
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• 2009

The present study was carried out to examine the sustained release effect of the implantable bovine somatotropin (SRI-BST) formula. In the blood profile test in steers, the bovine somatotropin concentration in serum by radioimmunoassay showed the peak concentration on the first day after the implantation of the SRI-BST formula, and concentration proceeded for 5 days (p < 0.05). The insulin-like growth factor-1 concentration showed the peak concentration on the seventh day after implantation of the SRIF-BST formula, and concentration proceeded for 10 days (p < 0.05). The glucose showed the peak concentration on the first day after implantation of the SRI-BST formula, and concentration continued for 3 days (p < 0.05). The blood urea nitrogen showed the lowest concentration on the third day after implantation of the SRI-BST formula, and concentration continued for 7 days (p < 0.05). These results proved that the SRIF-BST formula was the sustained release effects in steers.

• 멤브레인
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• 제3권2호
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• pp.70-78
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• 1993

글루코오즈(GOD) 옥시다제가 고정화된 PVA/키토산 플렌드막과 다공성 폴리아미드 복합막을 통해 인슐린의 투과거동을 살펴보았다. GOD가 고정화된 막을 통한 투과계수는 $10^{-6}{\sim}10^{-7}\textrm{cm}^3cm/\textrm{cm}^2sec$이었다. 복합막의 클루코오즈 농도에 대한 변화는 낮은 글루코오즈 농도에서 높았는데 이는 막으로부터 산소의 고갈 때문이었다. PVA/키토산 및 다공성 폴리아미드막을 통한 인슐린의 투과는 글루코오즈 농도에 따라 500mg%까지 점차 증가하였다.

• Journal of Pharmaceutical Investigation
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• 제38권3호
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• pp.177-182
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• 2008

The purposes of this study were to prepare dual-layered coated compact pellets containing three nutrients Glucose, Chromium picolinate, Vitamin C) for rumen bypass. The core compact pellets were prepared by an extrusionspheronization method and then double layered coated with pH independent EC (ethyl cellulose) and pH-dependent polymers ($Eudragit^{(R)}$ E100) using a fluid-bed spray coater. Depending on the coating levels of EC and $Eudragit^{(R)}$ E100, release profiles were variable in simulated rumen (pH 6.8) and abomasums (pH 2.0) fluid using USP apparatus I (basket method). When compact pellets were coated with EC (about 10% level in inner layer) and then $Eudragit^{(R)}$ E100 (20% level in outer layer) in a dual-layered manner, rumen-bypass delivery resisting rumen fluid followed by release in abomasums fluid could possible. The friability was also satisfactory based on chewing behavior of ruminants. The dual-layered coated compact pellets showed smooth surface and distinct inner/outer layers using scanning electron microscopy (SEM). The current rumen bypass delivery system can be also applicable to deliver other nutrients in ruminants.

• 동의생리병리학회지
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• 제22권6호
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• pp.1462-1469
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• 2008

The purpose of the study was to confirm what effect HRHDT treatment had on cell extinction by damage of endoplasmic reticulum induced to PC-12 cell damage by glucose deprivation. The study confirmed what effect it had on forming the condition of glucose deprivation within a culture fluid of PC-12 cell and on a nerve cell's survival rates and tested whether HRHDT could prevent extinction of PC-12 cell by glucose deprivation. Also, the study confirmed what effect HRHDT treatment had on the emitted quantity of LDH by glucose deprivation. To examine PC-12 cell's behavioral change under the condition of glucose deprivation and a protective effect of HRHDT on the change, the study observed PC-12 cell's behavioral change with a microscope. Also, the study confirmed density of calcium ion within cells followed by a culture time in the condition of glucose deprivation with FACS and confirmed what effect HRHDT treatment had on the above density of calcium ion within cells. Finally, the study carried out the western blot and confirmed what effect HRHDT treatment had on revelation of GRP 78 and CHOP protein and a segmental type of aspase 12. In this study, HRHDT rescued PC-12 cells from glucose deprivation-induced cell death. HRHDT also prevents the LDH release, Ca++ accumulation, and morphological change, which was associated with the ER stress. Furthermore, HRHDT reduced the expression of ER chaperone (Grp78 and CHOP) proteins by glucose deprivation in PC-12 cells. These results suggest that HRHDT might provide a useful therapeutic strategy in treatment of the neurodegenerative diseases caused by glucose deprivation injuries.

• 약학회지
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• 제41권6호
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• pp.782-788
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• 1997

This study was designed to characterize glucose-enhancing effects on endotoxin-induced prostaglandin production in primary cultured rat vascular smooth muscle cells (VSMC). High glucose treatment significantly augmented prostaglandin (PG) synthesis in lipopolysaccharide (LPS)-stimulated VSMC and this effect was maximal at the concentration of 4mg/ml. It has been reported that increases in glucose metabolism through sorbitol pathway could alter the cytosolic $NADH/NAD^+$ ratio and this change favors de novo synthesis of diacylglycerol (DAG) and, in turn. Results in the activation of protein kinase C (PKC) in vascular tissues. Protein kinase C (PKC) inhibitors, staurosporin and H7, blocked the glucose enhancing effect, and DAG, a PKC activator, significantly increased the PG production stimuated by LPS. Sodium pyruvate, which can reverse the alteration in cytosolic NADH/NAD+ ratio, reduced the high glucose effect on PG production. And also, zopolrestat, a strong aldose reductase inhibitor, almost completely blocked the augmentation effect of glucose on PG synthesis. Arachidonic acid release was significantly increased in high glucose treated group, which implied the increase in $PLA_2$ activity was associated with glucose enhancing effect. Metabloic, labeling study clearly showed that de novo synthesis of prostaglandin H synthase-2 (PGHS-2) is greatly increased in high glucose treated group and this was mitigated by the treatment of zopolrestat. Taken together, the activation of PKC through sorbitol pathway increased the activities of $PLA_2$ and PGHS which resulted in the augmentation in LPS-induced PG production in high glucose treated VSMC.

• 동의생리병리학회지
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• 제23권3호
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• pp.581-589
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• 2009

The water extract of Dohongsamul-tang(DHSMT) has been traditionally used in treatment of ischemic heart and brain diseases in Oriental Medicine. However, little is known about the mechanism by which DHSMT protects C6 glial cells from glucose deprevation induced damages. Therefore, this study was designed to evaluate the protective effects of DHSMT on 2-deoxy-D-glucose induced autophagy of C6 glial cells. Autophagic phenotype is evaluated by fluorescence microscopy and flow cytometry with specific biological staining dyes, including monodansylcadaverine and acridine orange, as well as Western blot analysis with microtubule-associated protein 1 light chain 3(LC3) and Beclin-1. Treatment with 2-deoxy-D-glucose significantly resulted in a decrease of the viability of C6 glial cells and increase of the extracellular LDH release in a dose and time-dependent manner. However, pretreatment with DHSMT protected C6 glial cells from glucose deprivation with 2-deoxy-D-glucose. The author also observed the fact that autophagy phenotype occurred by 2-deoxy-D-glucose in C6 glial cells. Pretreatment with 3-MA, a pharmacological inhibitior of autophagy, abolished the formation of acidic vesicle organelle in C6 glial cells treated with 2-deoxy-D-glucose. However, pretreatment with DHSMT inhibited the formation of autophagic phenotypes, including formation of acidic vesicle organelle, and increase of the expression of LC-3 II Beclin-1 proteins in C6 glial cells treated with 2-deoxy-D-glucose. Taken together, these data suggest that DHSMT is able to protect C6 glial cells from glucose deprivation with marked inhibition of autophagy formation.

• The Korean Journal of Physiology and Pharmacology
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• 제1권6호
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• pp.673-679
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• 1997

It has been generally accepted that glutamate mediates the ischemic brain damage, excitotoxicity, and induces release of neurotransmitters, including norepinephrine(NE), in ischemic milieu. In the present study, the role of nitric oxide(NO) in the ischemia-induced $[^3H]norepinephrine([^3H]NE)$ release from cortex slices of the rat was examined. Ischemia, deprivation of oxygen and glucose from $Mg^{2+}-free$ artificial cerebrospinal fluid, induced significant release of $[^3H]NE$ from cortex slices. This ischemia-induced $[^3H]NE$ release was significantly attenuated by glutamatergic neurotransmission modifiers. $N^G-nitro-L-arginine$ methyl ester(L-NAME), $N^G-monomethyl-L-arginine$ (L-NMMA) or 7-nitroindazole, nitric oxide synthase inhibitors attenuated the ischemia-evoked $[^3H]NE$ release. Hemoglobin, a NO chelator, and 5, 5- dimethyl-L-pyrroline-N-oxide(DMPO), an electron spin trap, inhibited $[^3H]NE$ release dose-dependently. Ischemia-evoked $[^3H]NE$ release was inhibited by methylene blue, a soluble guanylate cyclase inhibitor, and potentiated by 8-bromo-cGMP, a cell permeable cGMP analog, zaprinast, a cGMP phosphodiesterase inhibitor, and S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide generator. These results suggest that the ischemia-evoked $[^3H]NE$ release is mediated by NMDA receptors, and activation of NO system is involved.