• 제목/요약/키워드: Schisandra chinensis seed oil

검색결과 2건 처리시간 0.021초

LPS로 자극된 Raw 264.7 대식세포에서 오미자 씨앗오일의 항염증 효과 (Anti-inflammatory effect of seed oil of Schisandra chinensis in the LPS-treated RAW 264.7 macrophages)

  • 장재윤;박근혜
    • 대한본초학회지
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    • 제30권6호
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    • pp.77-82
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    • 2015
  • Objectives : This study was designed to investigate of the anti-inflammatory effects of Schisandra chinensis seed oil(SSO) on the production of pro-inflammatory substances in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages.Methods : SSO was measured the production of pro-inflammatory factor (NO, PGE2, IL-1β iNOS and, COX-2) in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. we used the following methods : cell viability assay, Griess reagent assay, enzyme-linked immunosorbent assay, Western blotting analysis.Results : The cell viability of SSO(0∼500 μl/mL) processing group was 96.9% and the processing of SSO didn't have an effect on the cytotoxicity. The inhibitory effect of the nitric oxide (no) production of SSO(500 μg/mL, 50 μg/mL, 10 μg/mL) was each 70.3%, 37.6% and 26.5%. IL-1β production inhibition ability of SSO(500 μg/mL, 100 μg/mL) was each 49.88% and 48.8%. PGE2 production inhibition ability of SSO(500 μg/mL, 100 μg/mL) was each 49.88% and 73.1%, 70.5%. By using SSO, it experimented about iNOS protein expression inhibition ability, that is the NO production enzyme. iNOS protein expression increased in the group processing LPS independently. iNOS protein expression decreased in the group processing SSO together. The expression of the COX-2 protein decreased 89.6%, 81.8% in the group processing SSO. The significance was in the relationship with NO formation inhibition with the relationship with the PGE2 formation inhibition and iNOS protein, it confirmed in SSO with the COX-2 protein.Conclusions : Stimulation of the RAW 264.7 cells with LPS caused an elevated production of nitric oxide (NO), IL-1β and PGE2 which was markedly inhibited by the pretreatment with SSO without causing any cytotoxic effects. The reduced expressions of iNOS protein were consistent with the reductions in NO production in the culture media. SSO may be useful for the treatment of various inflammatory diseases.

Activation of transient receptor potential vanilloid 3 by the methanolic extract of Schisandra chinensis fruit and its chemical constituent γ-schisandrin

  • Nam, Yuran;Kim, Hyun Jong;Kim, Young-Mi;Chin, Young-Won;Kim, Yung Kyu;Bae, Hyo Sang;Nam, Joo Hyun;Kim, Woo Kyung
    • The Korean Journal of Physiology and Pharmacology
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    • 제21권3호
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    • pp.309-316
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    • 2017
  • Transient receptor potential vanilloid 3 (TRPV3) is a non-selective cation channel with modest permeability to calcium ions. It is involved in intracellular calcium signaling and is therefore important in processes such as thermal sensation, skin barrier formation, and wound healing. TRPV3 was initially proposed as a warm temperature sensor. It is activated by synthetic small-molecule chemicals and plant-derived natural compounds such as camphor and eugenol. Schisandra chinensis (Turcz.) Baill (SC) has diverse pharmacological properties including antiallergic, anti-inflammatory, and wound healing activities. It is extensively used as an oriental herbal medicine for the treatment of various diseases. In this study, we investigated whether SC fruit extracts and seed oil, as well as four compounds isolated from the fruit can activate the TRPV3 channel. By performing whole-cell patch clamp recording in HEK293T cells overexpressing TRPV3, we found that the methanolic extract of SC fruit has an agonistic effect on the TRPV3 channel. Furthermore, electrophysiological analysis revealed that ${\gamma}$-schisandrin, one of the isolated compounds, activated TRPV3 at a concentration of $30{\mu}M$. In addition, ${\gamma}$-schisandrin (${\sim}100{\mu}M$) increased cytoplasmic $Ca^{2+}$ concentrations by approximately 20% in response to TRPV3 activation. This is the first report to indicate that SC extract and ${\gamma}$-schisandrin can modulate the TRPV3 channel. This report also suggests a mechanism by which ${\gamma}$-schisandrin acts as a therapeutic agent against TRPV3-related diseases.