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Your search keyword '"Jo, Il-Joo"' showing total 28 results
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28 results on '"Jo, Il-Joo"'

7. Poria cocos Extract from Mushrooms Stimulates Aquaporin-3 via the PI3K/Akt/mTOR Signaling Pathway

Author

Park,Sung-Gu, Jo,Il-Joo, Park,Seol-A, Park,Min-Cheol, Mun,Yeun-Ja, Park,Sung-Gu, Jo,Il-Joo, Park,Seol-A, Park,Min-Cheol, and Mun,Yeun-Ja

Abstract

Sung-Gu Park,1,* Il-Joo Jo,2,* Seol-A Park,3 Min-Cheol Park,1 Yeun-Ja Mun4 1Department of Oriental Medical Ophthalmology & Otolaryngology & Dermatology, College of Korean Medicine, Wonkwang University, Iksan, South Korea; 2Central Stroke Center of Korean medicine, College of Korean Medicine, Wonkwang University, Iksan, South Korea; 3Department of Beauty Design Graduate School, Wonkwang University, Iksan, South Korea; 4Department of Anatomy, College of Korean Medicine, Wonkwang University, Iksan, South Korea*These authors contributed equally to this workCorrespondence: Yeun-Ja Mun, Department of Anatomy, College of Korean Medicine, Wonkwang University, Iksan, South Korea, Tel +82-63-850-6942, Email yjmun@wku.ac.krBackground: Poria cocos (PC), a fungus, has been used for more than 2000 years as a food and medicine in China. PC and its components have various pharmacological effects on the skin, including immunomodulatory activities, barrier function improvement, and anti-tumor effects. However, the effect of PC in aquaporin-3 (AQP3) expression, which is essential for epidermal water permeability barrier maintenance, was not reported.Methods: This study examined the mechanism through which the ethanol extract of the sclerotium of PC (EPC) promoted the expression of AQP3 in cultured human keratinocytes. Western blotting was used to investigate the expression of AQPs and the activation of phosphoinositide 3-kinase (PI3K)/Akt-related signaling molecules in HaCaT cells. Cells were treated with inhibitors of PI3K/Akt and mechanistic target of rapamycin (mTOR) prior to EPC treatment.Results: EPC promoted the expression of AQP3 in HaCaT cells without affecting AQP1 and AQP2 expression. Phosphorylated Akt levels were increased by EPC treatment, and the inhibition of PI3K by LY2940002 resulted in a reduction in EPC-induced AQP3 expression. Furthermore, EPC stimulated the phosphorylation of p70S6K and AktSer473, which are downstream targets of mTO

Published
2022

22. Berberine ameliorates lipopolysaccharide-induced inflammatory responses in mouse inner medullary collecting duct-3 cells by downregulation of NF-κB pathway.

Author

Kim, Dong-Gu, Choi, Ji-Won, Jo, Il-Joo, Kim, Myoung-Jin, Lee, Ho-Sub, Hong, Seung-Heon, Song, Ho-Joon, Bae, Gi-Sang, and Park, Sung-Joo

Subjects
BERBERINE, DOWNREGULATION, WESTERN immunoblotting, CELLS
Abstract

The major role of inner medullary collecting duct (IMCD) cells is to maintain water and sodium homeostasis. In addition to the major role, it also participates in the protection of renal and systemic inflammation. Although IMCD cells could take part in renal and systemic inflammation, investigations on renal inflammation in IMCD cells have rarely been reported. Although berberine (BBR) has been reported to show diverse pharmacological effects, its anti-inflammatory and protective effects on IMCD cells have not been studied. Therefore, in the present study, we examined the anti-inflammatory and protective effects of BBR in mouse IMCD-3 (mIMCD-3) cells against lipopolysaccharide (LPS). An MTT assay was carried out to investigate the toxicity of BBR on mIMCD-3 cells. Reverse transcription quantitative-PCR and western blotting were performed to analysis pro-inflammatory molecules and cytokines. Mechanisms of BBR were examined by western blotting and immunocytochemistry. According to previous studies, pro-inflammatory molecules, such as inducible nitric oxide synthase and cyclooxygenase-2, and pro-inflammatory cytokines, such as interleukin (IL)-1β, IL-6 and tumor necrosis factor-α are increased in LPS-exposed mIMCD-3 cells. However, the production of these pro-inflammatory molecules is significantly inhibited by treatment with BBR. In addition, BBR inhibited translocation of nuclear factor (NF)-κB p65 from the cytosol to the nucleus, and degradation of inhibitory κ-Bα in LPS-exposed mIMCD-3 cells. In conclusion, BBR could inhibit renal inflammatory responses via inhibition of NF-κB signaling and ultimately contribute to amelioration of renal injury during systemic inflammation. [ABSTRACT FROM AUTHOR]

Published
2020
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