• Biomolecules & Therapeutics
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• v.23 no.5
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• pp.458-464
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• 2015

Sennoside A (erythro) and sennoside B (threo) are dianthrone glycosides and diastereomers. We investigated their abilities to prevent the gastric lesions associated with diseases, such as, gastritis and gastric ulcer. To elucidate their gastroprotective effects, the inhibitions of $HCl{\cdot}tOH$-induced gastritis and indomethacin-induced gastric ulcers were assessed in rats. It was observed that both sennoside A and sennoside B increased prostaglandin $E_2$ ($PGE_2$) levels and inhibited $H^+/K^+$-ATPase (proton pump). In a rat model, both compounds reduced gastric juice, total acidity and increased pH, indicating that proton pump inhibition reduces gastric acid secretion. Furthermore, sennoside A and B increased $PGE_2$ in a concentration-dependent manner. In a gastric emptying and intestinal transporting rate experiment, both sennoside A and sennoside B accelerated motility. Our results thus suggest that sennoside A and sennoside B possess significant gastroprotective activities and they might be useful for the treatment of gastric disease.

• Journal of Pharmaceutical Investigation
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• v.37 no.5
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• pp.291-295
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• 2007

Prostaglandin $E_1\;(PGE_1)$ was formulated as two self-microemulsifying drug delivery systems (SMEDDS) composed of Cremophor $EL^{(R)}$ or Cremophor $ELP^{(R)}$ as a surfactant, ethanol as a cosurfactant and Labrafac $CC^{(R)}$ as an oil to develop liquid preparation for the treatment of erectile dysfunction. In pseudo-ternary phase diagram, viscous gel area and microemulsion area were defined. In the measurement of viscosity, the viscosity of two formulations increased gradually upon the addition of water and it decreased from the water contents over 40%. With excessive water, the present systems formed a microemulsion spontaneously. From these results, rte could expect that the present liquid $PGE_1$ SMEDDS formulations might stay within the urethra in the viscous state when contacting the moisture of the urethra and can be easily eliminated by urination. In long-term stability study, we could select one formulation more stable at the shelf storage condition of $4^{\circ}C$.

• International Journal of Oral Biology
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• v.42 no.4
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• pp.149-153
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• 2017

Cyclooxygenase-2 (COX-2)-mediated prostaglandin $E_2$ ($PGE_2$) plays a key role in development and progression of inflammatory responses and Porphyromonas gingivalis is a common endodontic pathogen. In this study, we investigated induction of COX-2 and $PGE_2$ by P. gingivalis in human dental pulp cells (HDPCs). P. gingivalis increased expression of COX-2, but not that of COX-1. Increased levels of $PGE_2$ were released from P. gingivalis-infected HDPCs and this $PGE_2$ increase was blocked by celecoxib, a selective COX-2 inhibitor. P. gingivalis activated all three types of mitogen-activated protein kinases (MAPKs). P. gingivalis-induced activation of nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$) was demonstrated by the results of phosphorylation of $NF-{\kappa}B$ p65 and degradation of inhibitor of ${\kappa}B-{\alpha}$ ($I{\kappa}B-{\alpha}$). Pharmacological inhibition of each of the three types of MAPKs and $NF-{\kappa}B$ substantially attenuated P. gingivalis-induced $PGE_2$ production. These results suggest that P. gingivalis should promote endodontic inflammation by stimulating dental pulp cells to produce $PGE_2$.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.5
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• pp.1327-1333
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• 2006

Many traditional herbal remedies exhibit several beneficial effects including anti-inflammation. Panax notoginseng Buck F.H. Chen. is used as a therapeutic agent to stop haemorrhages and a tonic to promote health in Korean and Chinese medicine. The pharrnacokinetic profiles of the main P. notoginseng are still not accurately investigated. The exact mechanism of the anti-inflammatory action of P. notoginseng, however, has not been determined. In the present study, we examined the effect of P. notoginseng on lipopolysaccharide (LPS)-induced nitric oxide (NO) production, and inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) gene expression in RAW264.7 macrophages. The results indicated that P. notoginseng concentration-dependently inhibited LPS-induced NO production. Furthermore, P. notoginseng inhibited the expression of LPS-induced iNOS and COX-2 proteins without an appreciable cytotoxic effect on RAW264.7 cells. Berberine also inhibited LPS-induced iNOS protein as potently as P. notoginseng. This was consistent with the findings that P. notoginseng and also berberine inhibited prostaglandin E2 synthesis induced by LPS.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.5
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• pp.1295-1302
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• 2006

Our preliminary aim is to elucidate the pharmacokinetic features of the PNS(Panax notoginseng Buck F.H. Chen. (Arialiaceae) root). First, we assessed the prevention of neurtrophil functions. A Panax notoginseng inhibited neutrophil functions, including degranulation, superoxide generation, and leukotriene B4 production, without any effect on 5-lipoxygenase activity. This Panax notoginseng reduced nitric oxide (NO) and prostaglandin E2 production in mouse peritoneal macrophages stimulated with lipopolysaccharide, whereas no influence on the activity of inducible NO synthase, cyclo-oxygenase-2 or cyclo-oxygenase-1 was observed. Panax notoginseng significantly reduced mouse paw oedema induced by carrageenan. The results indicate that Panax notoginseng exerts anti-inflammatory effects related to the inhibition of neutrophil functions and of NO and prostaglandin E2 production, which could be due to a decreased expression of inducible NO synthase and cyclo-oxygenase-2.

• Journal of Microbiology and Biotechnology
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• v.29 no.10
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• pp.1675-1681
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• 2019

Clostridium difficile toxin A is known to cause colonic epithelial cell apoptosis, which is considered the main causative event that triggers inflammatory responses in the colon, reflecting the concept that the essential role of epithelial cells in the colon is to form a physical barrier in the gut. We previously showed that toxin A-induced colonocyte apoptosis and subsequent inflammation were dependent on prostaglandin E2 ($PGE_2$) produced in response to toxin A stimulation. However, the molecular mechanism by which $PGE_2$ mediates cell apoptosis in toxin A-exposed colonocytes has remained unclear. Here, we sought to identify the signaling pathway involved in toxin A-induced, $PGE_2$-mediated colonocyte apoptosis. In non-transformed NCM460 human colonocytes, toxin A exposure strongly upregulated expression of Bak, which is known to form mitochondrial outer membrane pores, resulting in apoptosis. RT-PCR analyses revealed that this increase in Bak expression was attributable to toxin A-induced transcriptional upregulation. We also found that toxin A upregulation of Bak expression was dependent on $PGE_2$ production, and further showed that this effect was recapitulated by an Prostaglandin E2(PGE2) receptor-1 receptor agonist, but not by agonists of other EP receptors. Collectively, these results suggest that toxin A-induced cell apoptosis involves $PGE_2$-upregulation of Bak through the EP1 receptor.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.50 no.1
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• pp.41-47
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• 2017

Perhaps the most common type of reproductive dysfunction in captive fish is failure of females to undergo final oocyte maturation and thus to ovulate and spawn. The success of aquaculture could therefore be improved by developing techniques to enhance natural spawning, artificial maturation, and/or to induce ovulation in farmed fish. This study aimed to investigate the effects of prostaglandin $E_2$ ($PGE_2$) and prostaglandin $F_{2{\alpha}}$ ($PGF_{2{\alpha}}$) on in vitro oocyte maturation (germinal vesicle breakdown, GVBD) and ovulation in the marine fish Chasmichthys dolichognathus. Post-vitellogenic follicles (0.80-0.94 mm diameter oocytes) were incubated with $PGE_2$ or $PGF_{2{\alpha}}$ at concentrations of 5, 50, or 500 ng/mL for 24 hours. A significant increase in GVBD was seen in 0.84 mm and 0.94 mm oocytes incubated with 50 ng/mL $PGE_2$ compared with the control. There was no significant increase in GVBD in any of the other experimental conditions (5 or 500 ng/mL $PGE_2$ or 5, 50, or 500 ng/mL $PGF_{2{\alpha}}$). Neither of the prostaglandins induced ovulation at the concentrations tested.These results suggest that GVBD was induced by incubation with 50 ng/mL $PGE_2$.

• The Korean Journal of Physiology
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• v.19 no.2
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• pp.173-187
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• 1985

Renal compensatory adaptation caused by ablation of a part of renal mass has long been known in the field of the compensatory renal hypertrophy or hyperplasia. Many reports were found on the chronic mechanisms on the compensatory renal hyperfunction after exclusion of the contralateral kidney. However the mechanism(s) of the acute compensatory hyperfunction after contralateral exclusion has not yet been clarified. In the present experiment, we have tried to prove the possibility of the involvement of the renin-angiotensin system and/or prostaglandin system in the control mechanism of the acute compensatory renal hyperfunction after contralateral kidney exclusion. There were found different responses of the renal hyperfunction by contralateral renal pedicle or ureteral occlusion. Contralateral renal pedicle or ureteral occlusion caused a sustained increases of the urinary volume, sodium and potassium excretion, while the magnitude of the changes was different quantitatively by the maneuvers. Blood collection affected on the acute compensatory renal responses after ureteral as well as renal pedicle occlusion. Plasma prostaglandin $E_2$ level was not changed by the contralateral renal pedicle or ureteral occlusion. Urinary excretion of Prostaglandin $E_2$, the indices of renal prostaglandin biosynthesis, was not changed by the contralateral renal pedicle occlusion, but increased without significance by the contralateral ureteral occlusion. Acute renal compensatory responses after contralateral renal pedicle occlusion were blocked by the pretreatment of indomethacin. Plasma renin activity increased after contralateral ureteral occlusion, but the pattern of the increases was the same as in the time-control group. Plasma renin activity after contralateral renal pedicle occlusion did not change by the time sequence. SQ 20,881, an angiotensin I converting enzyme inhibitor, blunted the contralateral renal responses after the renal pedicle occlusion. Bilateral renal denervation abolished the contralateral renal responses after the renal pedicle occlusion. The above data suggest that there is no direct evidence to support the involvement of the renin-angiotensin system and/or prostaglandin system for the acute compensatory renal hyperfunction after contralateral kidney exclusion, and that the functional changes of the intact kidney may be caused by a humoral substances, or other mechanisms by afferent renal nerve activity originating from the treated kidney.

• The Korean Journal of Physiology and Pharmacology
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• v.26 no.6
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• pp.405-413
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• 2022

Hair loss is a common status found among people of all ages. Since the role of hair is much more related to culture and individual identity, hair loss can have a great influence on well-being and quality of life. It is a disorder that is observed in only scalp patients with androgenetic alopecia (AGA) or alopecia areata caused by stress or immune response abnormalities. Food and Drug Administration (FDA)-approved therapeutic medicines such as finasteride, and minoxidil improve hair loss temporarily, but when they stop, they have a limitation in that hair loss occurs again. As an alternative strategy for improving hair growth, many studies reported that there is a relationship between the expression levels of prostaglandins (PGs) and hair growth. Four major PGs such as prostaglandin D2 (PGD2₂), prostaglandin I2 (PGI₂), prostaglandin E2 (PGE₂), and prostaglandin F2 alpha (PGF_2α) are spatiotemporally expressed in hair follicles and are implicated in hair loss. This review investigated the physiological roles and pharmacological interventions of the PGs in the pathogenesis of hair loss and provided these novel insights for clinical therapeutics for patients suffering from alopecia.

• Korean Journal of Acupuncture
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• v.22 no.1
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• pp.85-93
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• 2005

목적 : 본 연구는 봉독 약침액이 BV2 microglial cell에서 LPS로 유발된 염증반응에 대한 억제효과를 관찰하고자 하였다. 방법 : 봉독 약침액의 항염증작용을 관찰하기 위하여 BV2 microglial cell에 봉독약침액을 1시간전에 농도별$(0.1,\;1,\;100\;{\mu}g/ml)$로 전처치한 후 LPS $(5\;{\mu}g/ml)$로 24시간 동안 처리하여 RT-PCR, western blot, $PGE_2$, assay, NO synthesis assay등의 방법으로 관찰하였다. 결과 : LPS 염증유발에 의해서 BV2 microglial cell에서 COX-2 및 NOS 발현이 증가하였고, 이 러한 증가는 prostaglandin E2 및 NO 합성을 증가시켰다. 이에 반하여 봉독약침액으로 전처치한 군에서는 COX-2 및 NOS 발현을 억제시켜 결과적으로 prostaglandin 합성 및 NO 합성을 억제시킴을 확인할 수 있었다. 또한 LPS 염증유발에 의해서 활성화된 NF-kB의 발현을 억제 시켰다. 결론 : 봉독약침 액은 LPS 염증유발에 의해서 증가된 prostaglandin E2 및 NO 합성을 억제시킴으로써 여러 가지 염종질환의 치료에 유효한 효과가 있을 것으로 사려 된다.