• Journal of Microbiology and Biotechnology
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• 제22권11호
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• pp.1457-1466
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• 2012

Antimicrobial peptides (AMPs) exert antimicrobial activity against Gram-positive and Gram-negative bacteria, fungi, and viruses by various mechanisms. AMPs commonly possess particular characteristics by harboring cationic and amphipathic structures and binding to cell membranes, resulting in the leakage of essential cell contents by forming pores or disturbing lipid organization. These membrane disruptive mechanisms of AMPs are possible to explain according to the various structure forming pores in the membrane. Some AMPs inhibit DNA and/or RNA synthesis as well as apoptosis induction by reactive oxygen species (ROS) accumulation and mitochondrial dysfunction. Specifically, mitochondria play a major role in the apoptotic pathway. During apoptosis induced by AMPs, cells undergo cytochrome c release, caspase activation, phosphatidylserine externalization, plasma or mitochondrial membrane depolarization, DNA and nuclei damage, cell shrinkage, apoptotic body formation, and membrane blebbing. Even AMPs, which have been reported to exert membrane-active mechanisms, induce apoptosis in yeast. These phenomena were also discovered in tumor cells treated with AMPs. The apoptosis mechanism of AMPs is available for various therapeutics such as antibiotics for antibiotic-resistant pathogens that resist to the membrane active mechanism, and antitumor agents with selectivity to tumor cells.

• Journal of Plant Biology
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• 제36권4호
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• pp.383-389
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• 1993

Intact leaf과 detached epidermis에 있는 공변세포의 전기 생리학적 특성에 대한 빛과 이산화탄소의 효과를 조사하였다. 빛을 intact leaf의 abaxial side에 처리하면 공변세포막이 과분극 (hyperpolarization)되었다. 닭의장풀의 intact leaf에 있는 공변세포들은 빛에 의해 최대 13 mV 그리고 이산화탄소에 의해 42 mV까지 membrane potential difference(MPD)가 negative하게 변했다. 자주달개비에서도 비슷한 결과를 얻었다. 그러나, 빛과 이산화탄소를 detached epidermis에 있는 공변세포에 처리할 경우에는 공변세포의 MPD가 변하지 않았다. 위의 결과로부터, 엽육세포가 공변세포의 MPD 변화에 영향을 주는 것으로 사료되어, 엽육세포들을 광합성 억제제들을 침윤시켜 엽육세포 광합성의 어느 기작이 공변세포 MPD 변화에 영향을 주는지 조사하였다. CCCP로 침윤한 잎의 공변세포막은 적색광에 의해 약간 탈분극(depolarization)되었고, 이산화탄소에 의해 과분극되었다. 반면에, DCCD와 DCMU로 침윤한 경우에는 대조구 잎과 마찬자기로 적색광과 이산화탄소에 의해 과분극되었다. Azide로 침윤한 잎에 적색광을 처리하면 공변세포의MPD는 변하지 않았고, 이산화탄소를 처리하면 다른 처리구들에 비해 훨씬 감소한 막의 과분극을 보였다. 이는 azide가 잎에 손상을 유도하며 세포내 대사활성을 감소시킨 결과 이산화탄소에 의한 MPD 변화가 작았고, 적색광은 아무 효과도 보이지 않은 것으로 사료된다. 따라서, 엽육세포가 적색광을 감지하며 빛에 의해 유도된 공변세포막 과분극은 순환적 광인산화 반응에 의해 생성된 에너지에 의존하나 이산화타소에 의해 유도된 공변세포막 과분극은 광합성가 무관하다고 볼 수 있다. 또한 이산화탄소를 intact leaf에 처리하면 공변세포 액포가 알칼리화되는 것을 관찰하였는데, 이는 막의 과분극이 양성자 이온의 방출에 의해 일어난다는 것을 의미한다.

• The Korean Journal of Physiology and Pharmacology
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• 제7권4호
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• pp.231-238
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• 2003

The present study was undertaken to investigate the effect of bradykinin on secretion of catecholamines (CA) evoked by stimulation of cholinergic receptors and membrane depolarization from the isolated perfused model of the rat adrenal glands, and to elucidate its mechanism of action. Bradykinin $(3{\times}10^{-8}M)$ alone produced a weak secretory response of the CA. however, the perfusion with bradykinin $(3{\times}10^{-8}M)$ into an adrenal vein of the rat adrenal gland for 90 min enhanced markedly the secretory responses of CA evoked by ACh $(5.32{\times}10^{-3}M)$, excess $K^+$ ($5.6{\times}10^{-2}M$, a membrane depolarizer), DMPP ($10^{-4}$ M, a selective neuronal nicotinic agonist) and McN-A-343 ($10^{-4}$ M, a selective M1-muscarinic agonist). Moreover, bradykinin ($3{\times}10^{-8}$ M) in to an adrenal vein for 90 min also augmented the CA release evoked by BAY-K-8644, an activator of the dihydropyridine L-type $Ca^{2+}$ channels. However, in the presence of $(N-Methyl-D-Phe^7)$-bradykinin trifluoroacetate salt $(3{\times}10^{-8}M)$, an antagonist of $BK_2$-bradykinin receptor, bradykinin no longer enhanced the CA secretion evoked by Ach and high potassium whereas the pretreatment with Lys-$(des-Arg^9,\;Leu^9)$-bradykinin trifluoroacetate salt $(3{\times}10^{-8}M)$, an antagonist of $BK_1$-bradykinin receptor did fail to affect them. Furthermore, the perfusion with bradykinin $(3{\times}10^{-6}M)$ into an adrenal vein of the rabbit adrenal gland for 90 min enhanced markedly the secretory responses of CA evoked by excess $K^+$ $(5.6{\times}10^{-2}M)$. Collectively, these experimental results suggest that bradykinin enhances the CA secretion from the rat adrenal medulla evoked by cholinergic stimulation (both nicotininc and muscarinic receptors) and membrane depolarization through the activation of $B_2$-bradykinin receptors, not through $B_1$-bradykinin receptors. This facilitatory effect of bradykinin seems to be associated to the increased $Ca^{2+}$ influx through the activation of the dihydropyridine L-type $Ca^{2+}$ channels.

• 생명과학회지
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• 제18권11호
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• pp.1513-1520
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• 2008

4-Hydroxynonenal (4-HNE)는 세포내 레독스의 균형을 깨뜨려 혈관 기능 손상을 일으킨다. 본 연구자들은 HNE의 축적이 야기하는 혈관 기능 손상기전을 더 잘 이해하기 위하여 혈관 내피 세포의 미토콘드리아 세포사 메커니즘을 규명하였다. HNE를 처리한 세포에서는 미토콘드리아 막전위 소실과 그에 따른 cytochrome C의 방출이 유도되었으며, Bax의 증가 및 Bcl-2의 감소가 관찰되었다. ROS 제거제인 NAC와 peroxynitrite 제거제인 페니실라민은 HNE가 유도하는 ROS 생성을 차단하여 cytochrome C 방출과 세포사를 억제하였다. 세포에 HNE와 zVAD-fmk (caspase 저해제)를 같이 처리하면 HNE가 유도하는 세포사를 억제하지 못하는데 이는 HNE에 의한 세포사가 caspase에 비의존적 단계일 가능성을 시사하였다. 위의 결과들은 HNE가 유도하는 혈관 내피 세포의 세포사 매커니즘은 미토콘드리아 막전위의 탈분극에 의해 촉발되며 이는 혈관계 항상성의 악화와 노화에 의해 수반되는 혈관기능 손상을 유도할 것으로 사료된다.

• The Korean Journal of Physiology and Pharmacology
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• 제11권3호
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• pp.97-106
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• 2007

The present study was attempted to investigate the effect of nicorandil, which is an ATP-sensitive potassium ($K_{ATP}$) channel opener, on secretion of catecholamines (CA) evoked by cholinergic stimulation and membrane depolarization from the isolated perfused rat adrenal glands. The perfusion of nicorandil ($0.3{\sim}3.0mM$) into an adrenal vein for 90 min produced relatively dose-and time-dependent inhibition in CA secretion evoked by ACh (5.32 mM), high $k^+$ (a direct membrane depolarizer, 56 mM), DMPP (a selective neuronal nicotinic receptor agonist, $100{\mu}M$ for 2 min), McN-A-343 (a selective muscarinic $M_1$ receptor agonist, $100{\mu}M$ for 4 min), Bay-K-8644 (an activator of L-type dihydropyridine $Ca^{2+}$ channels, $10{\mu}M$ for 4 min) and cyclopiazonic acid (an activator of cytoplasmic $Ca^{2+}$-ATPase, $10{\mu}M$ for 4 min). In adrenal glands simultaneously preloaded with nicorandil (1.0 mM) and glibenclamide (a nonspecific $K_{ATP}$-channel blocker, 1.0 mM), the CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were recovered to the considerable extent of the control release in comparison with that of nicorandil-treatment only. Taken together, the present study demonstrates that nicorandil inhibits the adrenal CA secretion in response to stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by membrane depolarization from the isolated perfused rat adrenal glands. It seems that this inhibitory effect of nicorandil may be mediated by inhibiting both $Ca^{2+}$ influx and the $Ca^{2+}$ release from intracellular store through activation of $K_{ATP}$ channels in the rat adrenomedullary chromaffin cells. These results suggest that nicorandil-sensitive $K_{ATP}$ channels may play an inhibitory role in the regulation of the rat adrenomedullary CA secretion.

• 동의생리병리학회지
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• 제27권1호
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• pp.112-117
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• 2013

We studied the modulation of pacemaker activities by Samchulkunbi-tang (SCKB) in cultured interstitial cells of Cajal (ICC) from murine small intestine with the whole-cell patch-clamp technique. Externally applied SCKB produced membrane depolarization in the current-clamp mode. The pretreatment with $Ca^{2+}$-free solution and thapsigargin, a $Ca^{2+}$-ATPase inhibitor in endoplasmic reticulum, abolished the generation of pacemaker potentials and suppressed the SCKB-induced action. The application of flufenamic acid (a nonselective cation channel blocker) abolished the generation of pacemaker potentials by SCKB. However, the application of niflumic acid (a chloride channel blocker) did not inhibit the generation of pacemaker potentials by SCKB. In addition, the membrane depolarizations were inhibited by not only GDP-${\beta}$-S, which permanently binds G-binding proteins, but also U-73122, an active phospholipase C inhibitor. These results suggest that SCKB modulates the pacemaker activities by nonselective cation channels and external $Ca^{2+}$ influx and internal $Ca^{2+}$ release via G-protein and phospholipase C-dependent mechanism. Therefore, the ICC are targets for SCKB and their interaction can affect intestinal motility.

• The Korean Journal of Physiology
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• 제28권1호
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• pp.51-59
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• 1994

This study was carried out to elucidate the excitatory mechanisms of Substance P in the antral circular muscle, using isometric contraction recording, conventional microelectrode method and whole-cell patch clamp technique. Substance P produced tonic and phasic contractions in a dose-dependent manner and depolarized membrane potential with increased amplitude of slow waves in muscle strips. Voltage-dependent $Ca^{2+}$ currents were increased by the application of Substance P from a holding potential of -60mV to 50mV in 10mV steps and this effect was blocked by the addition of an antagonist. Also Substance P increased transient and spontaneous oscillatory $K^+$ outward currents. The enhanced outward currents were abolished by apamin in dispersed single cells. These results suggest that the depolarization of membrane potential by Substance P activates voltage-dependent $Ca^{2+}$ channels, which represents an excitatory response in the antral circular muscle and led to an increase in $Ca^{2+}\;activated\;K^+\;currents$.

• The Journal of Korean Physical Therapy
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• 제13권1호
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• pp.237-243
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• 2001

Skeletal muscle cells are activated by ${\alpha}$-motorneurons which release acetylcholine at the neuromuscular junction. This results in a local depolarization of surface membrane which triggers an action potential. The action potential propagates along the surface membrane and also into the T-tubule system. In the triads T-tubules are in close connection with the terminal cisternae of the sarcoplasmic reticulum(SR). The action potential activaies T-tubule voltage sensors(DHP receptors). which activates SR Ca$^{2+}$ release channels(ryanodinc receptors). Ca$^{2+}$ have a key role in skeletal muscle in that an increase of free myoplasmic Ca$^{2+}$ concentration. The process of coupling chemical and electrical signals at the cell surface to the intracellular release of Ca$^{2+}$and ultimate contraction of muscle fibers is termed excitation-contraction coupling(ECC). Coupling of cel1 surface signals to intracellular Ca$^{2+}$ release proceeds by several mechanisms in skeletal muscle cells. This review focus on sarcopiasmic reticulum(SR) Ca$^{2+}$ releasing mechanisms from sarcoplasmic reticulum in the skeletal muscle. The mechanisms include DCCR, CICR, and HCR.

• 대한한방부인과학회지
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• 제18권3호
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• pp.77-91
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• 2005

Purpose : Trichosanthis Radix is traditional medical herb which has been shown to inhibit tumor cell proliferation. In this study, the effects of Trichosanthis Radix extract were investigated on inducing growth inhibition and apoptosis of human uterine cervical carcinoma cells. Methods : Human uterine cervical carcinoma cells line, ME-180, was used for the study. The cells were treated with varying concentrations of Trichosanthis Radix extract. Cell growth and inhibitory rate were measured by MTT assay. Apoptosis induction was detected by fluorescence microscopy, DNA ladder formation and flow cytometry. Results : Trichosanthis Radix extract inhibited the growth of human uterine cervical carcinoma cells in a dose-dependent manner. It induced ME-180 cells to undergo apoptosis including fragmented nuclei and nucleosome-sized DNA fragmentation. Flow cytometric analysis showed the increasing rate of apoptotic cells by Trichosanthis Radix extract. Reduction of mitochondrial membrane potential and increase in caspase-3 activity and were found in ME-180 cells treated with Trichosanthis Radix extract. Conclusion : Our data suggest that Trichosanthis Radix extract inhibit the growth and proliferation of ME-180 cells by apoptotic induction and facilitates its activity via caspase-3 activation initiated by depolarization of mitochondria.

• 한국정보기술학회 영문논문지
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• 제10권2호
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• pp.199-214
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• 2020

An important technique of the present invention is primarily to parallel light detection, self-pulse therapy after diagnosis. Herpes zoster is a disease caused by varicella zoster virus, and the virus that has been latent in the dorsal root ganglion that controls the skin segment loses its immune system and physically damages it. It is an acute skin disease in which acute pain and bullous rash occur along the sensory ganglia, which are rehab by inducers such as malignant tumors. Dorsal root ganglion after complete recovery of varicella, relapsed after incubation in brain ganglion, latent virus sometimes suppressed activity by cell mediated immunity, and in cell ganglion with reduced cellular immunity. It proliferates and destroys neurons, causing pain while forming a rash and blisters. This can reduce cell necrosis and increase the phagocytosis and enzymatic activity through the movement of ions through the cell membrane, depolarization and membrane potential change, growth factor secretion, calcium ion transfer, chondrocyte synthesis, etc., And may offer treatment options for lesions of herpes zoster and post-herpetic neuralgia (PHN).Therefore, according to the present research, the diagnosis and treatment device of treating paing for herpes zoster and post-herpetic pain can be implemented in the early stage of herpes zoster, and conventional analgesic regulation, anti-inflammatory effect, post-herpetic neuralgia.