• 동의생리병리학회지
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• 제21권1호
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• pp.136-144
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• 2007

Biotae Orientalis has been widely used for treatment of relaxion of smooth muscle, gastrointestinal hemorrhage and alopecia in Oriental Medicine. This experiment examined the effect of an extracts, obtained from the acetone and MeOH extracts of dried or fresh Biotae Orientalis, on hair growing activity of the C57BL/6N mice after topical application to skin. First, We examined on hair growth activity of extracts of Biotae Orientalis compare to control and 1% minoxidil groups. Second, We investigated on the number of hair follicle and mast cells after topical application of extracts of the Biotae Orientalis to skin for 16 day. Third, We investigated immunoreactive density of vascular endothelial growth factor(VEGF), protein kinase C-${\alpha}$(PKC-${\alpha}$) and stem(mast) cell factor(SCF) in skin of C57BL/6N mice by immunohistochemical methods. I fourth investigated changes of subpopulation of splenocytes and thymocytes in C57BL/6N mice for 16day using laser flow cytometry. The results were as follows : Hair growing effect of acetone and MeOH extracts of dried and fresh Biotae Orientalis was observed in 70%, 90% and 60% in hair removed skin area in 16 day respectively. Immunoreactive density of VEGF and PKC-${\alpha}$ in skin of experimental groups was weakly stained compare to control group in 10 day. Immunoreactive density of stem cell factor in skin of experimental group was heavily stained compare to control group in 10 day. Splenic TH/TC Iymphocytes of lived MeOH extracts group significantly increased compare to control group. TH cells in thymic T lymphocytes were increased compare to control group. These experiment suggest that acetone and MeOH extracts of Biotae Orientalis may be used for topical treatment of alopecia areata.

• Tuberculosis and Respiratory Diseases
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• 제62권5호
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• pp.421-426
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• 2007

진행성 간질환의 합병증으로 발생하는 문맥폐고혈압은, 이차성 폐동맥고혈압 중에서 진행성 간질환에 의한 문맥고혈압과 연관된 폐동맥고혈압으로 분류되며, 독특한 임상적, 병태생리학적 특징을 보인다. 임상양상은 점진적인 운동성 호흡곤란, 흉통 등을 호소하지만, 증상 없이 우연히 발견되는 경우도 있다. 심초음파 검사를 통해 예비적으로, 우심장 도관삽입으로 직접 우심실 및 평균 폐동맥압을 측정하여 진단할 수 있다. 치료는 칼슘통로차단제, 프로스타노이드 등을 사용하지만, 근본적인 치료를 위해서는 간 및 폐이식을 고려해야 한다. 저자들은 53세 여자로 20년 전에 간경변을 진단받은 후 호흡곤란으로 내원한 환자에게서, 간경변의 원인으로 원발성 담관성 간경변을 진단하고, 호흡곤란의 원인으로 문맥폐고혈압을 진단하여 치료하였기에 문헌고찰과 함께 보고한다.

• 대한약리학회지
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• 제31권3호
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• pp.291-297
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• 1995

본 연구의 목적은 protein kinase C의 활성물질인 phorbol ester의 수축에 대한 cGMP 및 cAMP의 조절기전을 명확히 하기 위하여 흰쥐의 대동맥을 재료로 실험을 수행하였다. Sodium nitroprusside는 guanylyl cyclase를 활성화시켜 cGMP를, forskolin은 adenylyl cyclase를 활성화시켜서 cAMP를 증가시키는 것으로 보고되어 있으므로 위의 두 약물을 선택하였다. Phorbol ester는 시간경과와 함께 지속적인 수축을 발생하였으며 30분경 안정상태에 도달하였다. 동시에 20-kDa myosin light chain (MLC)의 인산화도 증가하였으며 30분경 최대치를 나타내었다. Sodium nitroprusside와 forskolin은 phorbol ester에 의한 수축을 농도의존적으로 억제하였으나 sodium nitroprusside가 forskolin보다 더욱 민감하게 억제하였다. Phorbol ester는 $^{45}Ca^{2+}$의 유입을 증가시켰고 sodium nitroprusside와 forskolin은 이 증가된 $^{45}Ca^{2+}$을 유의하게 억제하였다. Phorbol ester에 의하여 증가된 MLC의 인산화는 sodium nitroprusside 및 forskolin 각각의 최대농도로 억제되었다. 이상과 같은 결과로 볼때 아마도 cGMP와 cAMP는 phorbol ester에 의한 수축을 $^{45}Ca^{2+}$ 유입억제에 이은 MLC 인산화 억제에 의하여 이완작용을 나타내는 것으로 추측되며 cGMP가 cAMP보다 protein kinase C 매개의 수축조절에 더 중요하게 작용하리라 추측된다.

• The Korean Journal of Physiology and Pharmacology
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• 제3권4호
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• pp.415-425
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• 1999

$[K^+]_o$ can be increased under a variety of conditions including subarachnoid hemorrhage. The increase of $[K^+]_o$ in the range of $5{\sim}15$ mM may affect tensions of blood vessels and cause relaxation of agonist-induced precontracted vascular smooth muscle $(K^+-induced$ relaxation). In this study, effect of the increase in extracellular $K^+$ concentration on the agonist-induced contractions of various arteries including resistant arteries of rabbit was examined, using home-made Mulvany-type myograph. Extracellular $K^+$ was increased in three different ways; from initial 1 to 3 mM, from initial 3 to 6 mM, or from initial 6 to 12 mM. In superior mesenteric arteries, the relaxation induced by extracellular $K^+$ elevation from initial 6 to 12 mM was the most prominent among the relaxations induced by the elevations in three different ways. In cerebral arteries, the most prominent relaxation was produced by the elevation of extracellular $K^+$ from initial 1 to 3 mM and a slight relaxation was provoked by the elevation from initial 6 to 12 mM. In superior mesenteric arteries, $K^+-induced$ relaxation by the elevation from initial 6 to 12 mM was blocked by $Ba^{2+}\;(30\;{\mu}M)$ and the relaxation by the elevation from 1 to 3 mM or from 3 to 6 mM was not blocked by $Ba^{2+}.$ In cerebral arteries, however, $K^+-induced$ relaxation by the elevation from initial 3 to 6 mM was blocked by $Ba^{2+},$ whereas the relaxation by the elevation from 1 to 3 mM was not blocked by $Ba^{2+}.$ Ouabain inhibited all of the relaxations induced by the extracellular $K^+$ elevations in three different ways. In cerebral arteries, when extracellular $K^+$ was increased to 14 mM with 2 or 3 mM increments, almost complete relaxation was induced at 1 or 3 mM of initial $K^+$ concentration and slight relaxation occurred at 6 mM. TEA did not inhibit $Ba^{2+}-sensitive$ relaxation at all and NMMA or endothelial removal did not inhibit $K^+-induced$ relaxation. Most conduit arteries such as aorta, carotid artery, and renal artery were not relaxed by the elevation of extracellular $K^+.$ Among conduit arteries, trunk of superior mesenteric artery and basilar artery were relaxed by the elevations of $[K^+]_o.$ These data suggest that $K^+-induced$ relaxation has two independent components, $Ba^{2+}-sensitive$ and $Ba^{2+}-insensitive$ one and there are different mechanisms for $K^+-induced$ relaxation in various arteries.

• The Korean Journal of Pain
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• 제29권4호
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• pp.229-238
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• 2016

Background: The goal of this in vitro study was to investigate the effect of lipid emulsion on vasodilation caused by toxic doses of bupivacaine and mepivacaine during contraction induced by a protein kinase C (PKC) activator, phorbol 12,13-dibutyrate (PDBu), in an isolated endothelium-denuded rat aorta. Methods: The effects of lipid emulsion on the dose-response curves induced by bupivacaine or mepivacaine in an isolated aorta precontracted with PDBu were assessed. In addition, the effects of bupivacaine on the increased intracellular calcium concentration ($[Ca^{2+}]_i$) and contraction induced by PDBu were investigated using fura-2 loaded aortic strips. Further, the effects of bupivacaine, the PKC inhibitor GF109203X and lipid emulsion, alone or in combination, on PDBu-induced PKC and phosphorylation-dependent inhibitory protein of myosin phosphatase (CPI-17) phosphorylation in rat aortic vascular smooth muscle cells (VSMCs) was examined by western blotting. Results: Lipid emulsion attenuated the vasodilation induced by bupivacaine, whereas it had no effect on that induced by mepivacaine. Lipid emulsion had no effect on PDBu-induced contraction. The magnitude of bupivacaine-induced vasodilation was higher than that of the bupivacaine-induced decrease in $[Ca^{2+}]_i$. PDBu promoted PKC and CPI-17 phosphorylation in aortic VSMCs. Bupivacaine and GF109203X attenuated PDBu-induced PKC and CPI-17 phosphorylation, whereas lipid emulsion attenuated bupivacaine-mediated inhibition of PDBu-induced PKC and CPI-17 phosphorylation. Conclusions: These results suggest that lipid emulsion attenuates the vasodilation induced by a toxic dose of bupivacaine via inhibition of bupivacaine-induced PKC and CPI-17 dephosphorylation. This lipid emulsion-mediated inhibition of vasodilation may be partly associated with the lipid solubility of local anesthetics.

• Molecules and Cells
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• 제40권6호
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• pp.386-392
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• 2017

Periodontal ligament stem cells (PDLSCs) are multipotent stem cells derived from periodontium and have mesenchymal stem cell (MSC)-like characteristics. Recently, the perivascular region was recognized as the developmental origin of MSCs, which suggests the in vivo angiogenic potential of PDLSCs. In this study, we investigated whether PDLSCs could be a potential source of perivascular cells, which could contribute to in vivo angiogenesis. PDLSCs exhibited typical MSC-like characteristics such as the expression pattern of surface markers (CD29, CD44, CD73, and CD105) and differentiation potentials (osteogenic and adipogenic differentiation). Moreover, PDLSCs expressed perivascular cell markers such as NG2, ${\alpha}-smooth$ muscle actin, platelet-derived growth factor receptor ${\beta}$, and CD146. We conducted an in vivo Matrigel plug assay to confirm the in vivo angiogenic potential of PDLSCs. We could not observe significant vessel-like structures with PDLSCs alone or human umbilical vein endothelial cells (HUVECs) alone at day 7 after injection. However, when PDLSCs and HUVECs were co-injected, there were vessel-like structures containing red blood cells in the lumens, which suggested that anastomosis occurred between newly formed vessels and host circulatory system. To block the $SDF-1{\alpha}$ and CXCR4 axis between PDLSCs and HUVECs, AMD3100, a CXCR4 antagonist, was added into the Matrigel plug. After day 3 and day 7 after injection, there were no significant vessel-like structures. In conclusion, we demonstrated the perivascular characteristics of PDLSCs and their contribution to in vivo angiogenesis, which might imply potential application of PDLSCs into the neovascularization of tissue engineering and vascular diseases.

• 대한수의학회지
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• 제39권5호
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• pp.930-937
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• 1999

Atrial natriuretic peptide(ANP) is a hormone with potent natriuretic, diuretic and relaxing properties on vascular smooth muscle. Specific chemical modulator in response for the ANP secretion has not been found yet. Therefore, we have investigated the role of $Ca^{2+}$ responsible for the regulation of ANP induced by protein kinase C(PKC) on mechanically stretch-induced ANP secretion in the rat atria. The results obtained were as follows ; 1. ANP secretion and ANP concentration were increased to more in $Ca^{2+}$-free buffer than in the Kreb-Henseleit buffer on mechanically stretch-induced ANP secretion(p < 0.05), but extracellular fluid translocation(ECF) was not significant. Phorbol 12-myristate 13-acetate(PMA, $10^{-7}M$) induced ANP secretion and ANP concentration in $Ca^{2+}$-free buffer shown to more accentuate on mechanically stretch-induced ANP secretion than in the $Ca^{2+}$-free buffer(p < 0.05), but ECF translocation was not significant. 2. In the presence of ryanodine($3{\times}10^{-6}M$), PMA($10^{-7}M$) induced ANP secretion and ANP concentration in the Kreb-Henseleit buffer were shown to more increase on mechanically stretch-induced ANP secretion than in the ryanodine($3{\times}10^{-6}M$) with the Kreb-Henseleit buffer(p < 0.05), but ECF translocation was not significant. 3. In the presence of ryanodine($3{\times}10^{-6}M$), PMA($10^{-7}M$) induced ANP secretion and ANP concentration in the $Ca^{2+}$-free buffer was shown to more increase on mechanically stretch-induced ANP secretion than in the ryanodine($3{\times}10^{-6}M$) with the $Ca^{2+}$-free buffer on mechanically induced ANP secretion(p < 0.05), but ECF translocation was not significant. The results suggest that PKC-induced ANP secretion may not be related to the change of $Ca^{2+}$ on mechanically induced ANP secretion in the rat atria.

• Asian Pacific Journal of Cancer Prevention
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• 제16권3호
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• pp.1123-1127
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• 2015

Uterine leiomyomas (ULM), are benign tumors of the smooth muscle cells of the myometrium. They represent a common health problem and are estimated to be present in 30-70% of clinically reproductive women. Abnormal angiogenesis and vascular-related growth factors have been suggested to be associated with ULM growth. The angiotensin-I converting enzyme (ACE) is related with several tumors. The aim of this study was to identify possible correlation between ULM and the ACE I/D polymorphism, to evaluate whether the ACE I/D polymorphism could be a marker for early diagnosis and prognosis. ACE I/D was amplified with specific primer sets recognizing genomic DNA from ULM (n=72) and control (n=83) volunteers and amplicons were separated on agarose gels. The observed genotype frequencies were in agreement with Hardy-Weinberg equilibrium ($x^2=2.162$, p=0.339). There was no association between allele frequencies and study groups ($x^2=0.623$; p=0.430 for ACE I allele, $x^2=0.995$; p=0.339 for ACE D allele). In addition, there were no significant differences between ACE I/D polymorphism genotype frequencies and ULM range in size and number ($X^2=1.760;$ p=0.415 for fibroid size, $X^2=0.342;$ p=0.843 for fibroid number). We conclude that the ACE gene I/D polymorphism is not related with the size or number of ULM fibroids in Turkish women. Thus it cannot be regarded as an early diagnostic parameter nor as a risk estimate for ULM predisposition.

• 대한물리치료과학회지
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• 제13권2호
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• pp.99-119
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• 2006

Endothelin (ET) is a 21 amino acid peptide with multifunctional effects on the vasculature as well as a variety of other cell types such as respiratory, gastrointestinal, urogenital, endocrine, central nervous systems, and others. Endothelin has emerged as a modulator by autocrine and paracrine actions for many cellular activities, including vasoconstriction, cell proliferation, hormone production, neurotransmitter and/or neuromodulator. The endothelin family consists of three closely related peptides, ET-1, ET-2, and ET-3 derived from separate genes, such as chromosome 6, 1, and 20, respectively. ET-1 is the predominant isoform produced in the cardiovascular system and about which most is known. Endothelin receptors are seven-transmembrane GTP-binding protein-coupled receptors, which are classified into endothelin-A (ETA) and endothelin-B (ETB) receptors. Interestingly, recent evidence is accumulating to suggest that ET -1 may contribute to a variety of pain states such as allodynia and hyperalgesia in animals and humans. Therefore, in this review the biological characteristics and contraction-related mechanism of endothelin-1 in mammalian cells will be summarized. Especially, we focus on multifunctional roles for ET-1 in noxious stimulation-induced pain for the study of pain specialized physical therapy.

• The Korean Journal of Physiology and Pharmacology
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• 제17권3호
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• pp.181-187
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• 2013

Reactive oxygen species (ROS) are generated in various cells, including vascular smooth muscle and endothelial cells, and regulate ion channel functions. $K_{Ca}3.1$ plays an important role in endothelial functions. However, the effects of superoxide and hydrogen peroxide radicals on the expression of this ion channel in the endothelium remain unclear. In this study, we examined the effects of ROS donors on $K_{Ca}3.1$ expression and the $K^+$ current in primary cultured human umbilical vein endothelial cells (HUVECs). The hydrogen peroxide donor, tert-butyl hydroperoxide (TBHP), upregulated $K_{Ca}3.1$ expression, while the superoxide donors, xanthine/xanthine oxidase mixture (X/XO) and lysophosphatidylcholine (LPC), downregulated its expression, in a concentration-dependent manner. These ROS donor effects were prevented by antioxidants or superoxide dismustase. Phosphorylated extracellular signal-regulated kinase (pERK) was upregulated by TBHP and downregulated by X/XO. In addition, repressor element-1-silencing transcription factor (REST) was downregulated by TBHP, and upregulated by X/XO. Furthermore, $K_{Ca}3.1$ current, which was activated by clamping cells with 1 ${\mu}M$ $Ca^{2+}$ and applying the $K_{Ca}3.1$ activator 1-ethyl-2-benzimidazolinone, was further augmented by TBHP, and inhibited by X/XO. These effects were prevented by antioxidants. The results suggest that hydrogen peroxide increases $K_{Ca}3.1$ expression by upregulating pERK and downregulating REST, and augments the $K^+$ current. On the other hand, superoxide reduces $K_{Ca}3.1$ expression by downregulating pERK and upregulating REST, and inhibits the $K^+$ current. ROS thereby play a key role in both physiological and pathological processes in endothelial cells by regulating $K_{Ca}3.1$ and endothelial function.