• 생명과학회지
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• 제22권4호
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• pp.516-523
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• 2012

본 연구는 비만과 노화가 동시에 유발된 흰쥐에서 12주간의 트레드밀 운동과 L-arginine의 투여가 복부지방량, GH, IGF-I, somatostatin, fibrinogen, PAI-1에 미치는 영향을 관찰하고 이를 개선하는데 더욱 효과적인 방법을 제시하는데 그 목적이 있다. 이를 위해 단독 처치 군과 복합 처치 군으로 나누어 실험하여 그 효과를 비교, 분석한 결과 다음과 같은 결론을 얻었다. 1. 복부지방량은 통제집단에 비해 모든 집단에서 유의하게 감소하였다($p$<0.01). 2. AG+EX, AG+LA+EX집단에서 통제집단에 비해 GH의 혈중 농도가 유의하게 높게 나타났다($p$<0.1). 3. AG+EX, AG+LA+EX집단에서 통제집단에 비해 IGF-I의 혈중 농도가 유의하게 증가하였다($p$<0.01).

• 약학회지
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• 제38권1호
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• pp.24-30
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• 1994

Nitric oxide(NO) synthase was identified and characterized by determining the L-citrulline formed in the NO-Arg pathway in pancreatic tissues. NO synthase activities in chicken pancreas were dependent upon the concentration of L-Arg which is the substrate molecule for the NO synthase, the amount of the enzyme protein used, and linearly on the incubation time. NO synthase in mouse pancreas was found to be constitutive, not induced by lipopolysaccharide treatment. In vitro NO synthase activities of chicken pancreas were inhibited 36%, 21%, 12% and 44% by $200\;{\mu}M$ of MMA, DMA, D'MA and NAME respectively. These results suggest the presence of NO and NO synthase in the pancreas.

• The Korean Journal of Pain
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• 제35권4호
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• pp.413-422
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• 2022

Background: The neocortex, including the medial prefrontal cortex (mPFC), contains many neurons expressing nitric oxide synthase (NOS). In addition, increasing evidence shows that the nitric oxide (NO) and opioid systems interact in the brain. However, there have been no studies on the interaction of the opioid and NO systems in the mPFC. The objective of this study was to investigate the effects of administrating L-arginine (L-Arg, a precursor of NO) and N(gamma)-nitro-L-arginine methyl ester (L-NAME, an inhibitor of NOS) into the mPFC for neuropathic pain in rats. Also, we used selective opioid receptor antagonists to clarify the possible participation of the opioid mechanism. Methods: Complete transection of the peroneal and tibial branches of the sciatic nerve was applied to induce neuropathic pain, and seven days later, the mPFC was cannulated bilaterally. The paw withdrawal threshold fifty percent (50% PWT) was recorded on the 14th day. Results: Microinjection of L-Arg (2.87, 11.5 and 45.92 nmol per 0.25 µL) increased 50% PWT. L-NAME (17.15 nmol per 0.25 µL) and naloxonazine (an antagonist of mu opioid receptors, 1.54 nmol per 0.25 µL) inhibited anti-allodynia induced by L-Arg (45.92 nmol per 0.25 µL). Naltrindole (a delta opioid receptor antagonist, 2.45 nmol per 0.25 µL) and nor-binaltorphimine (a kappa opioid receptor antagonist, 1.36 nmol per 0.25 µL) were unable to prevent L-Arg (45.92 nmol per 0.25 µL)-induced antiallodynia. Conclusions: Our results indicate that the NO system in the mPFC regulates neuropathic pain. Mu opioid receptors of this area might participate in pain relief caused by L-Arg.

• 대한의생명과학회지
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• 제18권4호
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• pp.420-427
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• 2012

Sprague-Dawley (SD) rats were orally administered with NG-nitro-L-arginine methyl ester (L-NAME), which inhibits or blocks the production of nitric oxide from L-arginine in vascular endothelial cells and vessel tissue. We examined the effects of nitric oxide on some physiological changes such as blood pressure and heart rate, and confirms the apoptosis induced by the suppressed nitric oxide activity in the kidney. This study was performed to investigate correlation between the activities of nitric oxide and apoptosis by immunohistochemical changes of apoptotic control proteins with regulated chronic inhibition of nitric oxide. In the kidney from L-NAME-treated group, immunohistochemical reaction to the antigens of apoptosis inhibiting proteins such as bcl-2 and bcl-xL, exhibited a time-dependent reduction. The expression of apoptosis-inhibiting proteins such as bax and p53 increased expression in proportion to the duration of treatment. The most sensitive apoptosis regulating proteins to L-NAME were p53 in stimulation and bcl-2 in inhibition, respectively.

• Applied Biological Chemistry
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• 제48권4호
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• pp.411-417
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• 2005

마우스 대식세포주인 RAW264.7 세포에서 곽향(Agastache rugosa)을 포함한 21종의 한약재에서 제조한 열수추출물의 NO생산에 대한 조절효과를 조사하였다. 모든 한약재 추출물은 LPS자극으로 생산된 NO에 대하여 뚜렷한 소거활성을 보이지 않았으나, LPS 무처리 조건에서 곽향이 RAW264.7 세포의 NO생산을 강력하게 유도하였다. $200{\mu}M$의 NOS2의 저해제인 $N^G-monomethyl-L-arginine(N^GMMA$)의 처리에 의하여 곽향이 유도하는 NO 생산은 유의적으로 감소되었다. 또한 $NF-{\kappa}B$ 저해제인 pyrrolidine dithiocarbamate(PDTC)의 처리로 NO 생산이 $100{\mu}M$에서 약 79%까지 감소하였다. 이상의 실험 결과는 곽향 열수추출물이 RAW264.7 세포의 NOS2 발현의 이차적인 세포 내 신호를 발생시킬 수 있으며, NO는 L-arginine 의존적 경로에 의하여 생성된다는 사실을 시사하였다.

• Archives of Pharmacal Research
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• 제21권2호
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• pp.128-134
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• 1998

Nitric oxide synthase, NOS (EC.1.14.13.39), was purified from bovine pancreas over 5,500-fold with a 7.6% yield using 30% ammonium sulfate precipitation, and $2^1$,$5^1$-ADP-agarose and calmodulin-agarose affinity chromatography. The purified bovine pancreatic NOS (bpNOS) showed a single band on SDS-PAGE corresponding to an apparent molecular mass of 160 kDa, whereas it was 320 kDa on non-denaturating gel-filtration. This indicated a homodimeric nature of the enzyme. The specific activity of the purified bpNOS was 31.67 nmol L-citrulline fored/mtn/mg protein and an apparent $K\textrm{m}$ for L-arginine was 15.72 $\mu\textrm{M}$, The enzyme activity was dependent on $Ca^{2+}$ and calmodulin, and to a lesser extent on NADPH, FAD and FMN. $H_4B$ was not required as a cofactor for the activity. In an inhibition experiment with L-arginine analogues, $N^G$-nitro-L-arginine (NNA) had the most potent inhibitory effect on bpNOS, and $N^{G}$, $N^{G1}$-dimethyl-L-arginine (symmetric; sDMA) did not have any inhibitory effect. Immunohistochemical analysis of the bovine pancreas using brain type NOS antibody (anti-bNOS antibody) revealed that acinar cells showed strong immunoreactivity against the antibody.

• Biomolecules & Therapeutics
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• 제7권2호
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• pp.105-111
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• 1999

Nitric oxide (NO), a cellular messenger synthesized from L-arginine by NO synthase (NOS, EC.1.14.13.39), is considered to be a regulator of gastric secretion. In the present study, the role of NO in the regulation of exocrine secretion was investigated in rat gastric chief cells. Treatment of chief cells with carba-chol resulted in an increase in the arginine conversion to citrulline, the amount of $NO_{x}$, the release of pepsine-gen, and the level of cGMP Especially, carbachol-stimulated increase of arginine to citrulline transformation, the amount of $NO_{x}$, cGMP level and the release of pepsinogen were partially reduced by the natural NOS inhibitor, $N^{G}$-monomethyl-L-arginine (MMA) and $N^{G}$, $N^{G}$-dimethyl-L-arginine (DMA). Furthermore, MMA- and DMA-induced decrease of pepsinogen secretion showed dose-dependent patters. Activation of NOS is one of the early events in receptor-mediated cascade of reactions in gastric chief cells and NO, not completely, but partially mediates gastric secretion. Agonist-stimulated pepsinogen secretion in chief cells has been considered to be mediated in adenosine 3',5'-cyclic monophosphate pathway and/or guanosine 3', 5'-cyclic monophosphate (cGMP) pathway. Taken together, the above results suggest that partial decrease of exocrine secretion following treatment of NOS inhibitor may result from the inactivation of NOS and subsequent guano- late cyclase, and NO/cGMP pathway may play a pivotal role in exocrine secretion.

• 한국식품영양과학회지
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• 제44권9호
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• pp.1264-1269
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• 2015

본 연구에서는 누룩에서 ornithine 생성능을 보유하고 있는 Pediococcus 속 균주를 동정하고, ornithine 생성 유산균인 Pediococcus pentosaceus TNO-4를 이용하여 막걸리를 제조하였다. Ornithine의 전구물질인 arginine과 Pediococcus pentosaceus TNO-4를 첨가하여 제조한 ornithine 함유 막걸리의 ornithine 함량을 측정하고 세포 수준에서의 지방구 형성 억제 효과를 통한 항비만 효과를 평가하였다. Ornithine 막걸리의 ornithine 함량은 일반 막걸리에 비하여 3배 증가되었으며, 세포 실험 결과 0.05 mg/mL 농도의 ornithine 막걸리를 3T3-L1 세포에 처리하였을 때 독성이 없는 수준에서 유의적으로 지방구 형성을 억제하는 것을 관찰하였다. 본 연구를 바탕으로 후속 연구가 이루어진다면 기능성 물질이 강화된 우리나라 전통술인 막걸리를 통하여 지질축적 억제를 통한 항비만 효과를 기대해 볼 수 있을 것이라 사료된다. 더 나아가서 기능성이 부각된 막걸리의 개발을 통하여 막걸리 시장에 새로운 판로를 개척할 수 있고, 누룩에서 분리된 ornithine 생성능을 가진 유산균은 막걸리 이외에 여러 가지 발효식품에도 활용될 수 있을 것으로 기대된다.

• The Journal of Korean Physical Therapy
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• 제15권2호
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• pp.146-156
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• 2003

Isolated rat thoracic aorta which is pharmacologically precontracted by phenylephrine induces photorelaxation when exposed to long wave length UV-light. The aim of the present study was to characterize the mechanism of UV-light induced by photorelaxation in the rat aorta. 1. UV light relaxed both endothelium-intact and -denuded rat aortic rings contracted by phenylephrine. The magnitude of relaxation on UV light was dependent on the exposure time and slightly greatly in endothelium-denuded rings than in endothelium-intact preparations. 2. L-NAME (10 nM - 100 $\mu$M) but not D-NAME completely inhibited the photorelaxation in a concentration dependent manner. 3. The UV-induced relaxation was inhibited by methylene blue (1 - 100 uM), and verapamil (100 nM), and removal of extracellular $Ca^{2+}$. In contrast, UV-light induced photorelaxation was potentiated by $N^{w}$-nitro-L-arginine (L-NNA) treatment. These results suggest that UV light-induced photorelaxation may be due to nitric oxide from exogenously administered L-arginine as well as endogenous nitric oxide donors such as amino acid and arginine derivatives

• BMB Reports
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• 제28권2호
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• pp.124-128
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• 1995

Biodegradative threonine dehydratase purified from Serratia marcescens ATCC 25419 was inactivated by the arginine specific modification reagent, phenylglyoxal (PGO) and the lysine modification reagent, pyridoxal 5'-phosphate (PLP). The inactivation by PGO was protected by L-threonine and L-serine. The second order rate constant for the inactivation of the enzyme by PGO was calculated to be 136 $M^{-1}min^{-1}$. The reaction order with respect to PGO was 0.83. The inactivation of the enzyme by PGO was reversed upon addition of excess hydroxylamine. The inactivation of the enzyme by PLP was protected by L-threonine, L-serine, and a-aminobutyrate. The second order rate constant for the inactivation of the enzyme by PLP was 157 $M^{-1}min^{-1}$ and the order of reaction with respect to PLP was 1.0. The inactivation of the enzyme by PLP was reversed upon addition of excess acetic anhydride. Other chemical modification reagents such as N-ethylmaleimide, 5,5'-dithiobis (2-nitrobenzoate), iodoacetamide, sodium azide, phenylmethyl sulfonylfluoride and diethylpyrocarbonate had no effect on the enzyme activity. These results suggest that essential arginine and lysine residues may be located at or near the active site.