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Food-Borne Enterococci and Their Resistance to Oxidative Stress
arbora Vlková,Tomáš Szemes,Gabriel Minárik,Lubomíra Tóthová,Hana Drahovská,Ján Turňa,Peter Celec 한국미생물학회 2011 The journal of microbiology Vol.49 No.4
Enterococci are important food-borne pathogens that cause serious infections. Several virulence factors have been described including aggregation substance, gelatinase, cytolysin, and enterococcal surface protein. The ability to cause infections is mainly dependent on the response to oxidative stress due to the production of reactive oxygen species by immune cells. The aim of our study was to analyze the resistance of enterococcal strains from food to clinically relevant antiseptic agents with regard to the presence of selected virulence factors, and to uncover potential mechanisms of the antioxidative resistance. Eighty-two enterococcal isolates from Bryndza cheese were tested using in vitro growth assays to study the ability of these isolates to survive exposure to antiseptic agents – hydrogen peroxide, hypochlorite, and chlorhexidine. Virulence genotypes of the isolates were determined by PCR, and RT real time PCR was used for gene expression under oxidative stress. Resistance against antiseptic agents depends on the concentration of applied chemicals, on the time of exposure, but also on virulence factors of the enterococcal strains. Oxidative stress induces the expression of antioxidative enzymes and down-regulates the expression of prooxidative enzymes. These effects are dependent on the virulence genotype of the enterococcal strains. These findings are important for future research,especially concerning the role of enterococci in oral diseases.
헤어리베치 종자의 침지처리와 종피 파상 및 황산처리가 발아에 미치는 영향
김민태(Min-Tae Kim),이용환(Yong-Hwan Lee),전원태(Weon-Tai Jeon),김숙진(Sook Jin Kim),윤다해(Da-Hae Yun),구자환(Ja-Hwan Ku),송하나(Hana Song),이현복(Hyeon Bok Lee),서명철(Myung Chul Seo),강항원(Hang-Won Kang) 한국토양비료학회 2013 한국토양비료학회지 Vol.46 No.1
헤어리베치와 같은 두과 녹비작물은 종피가 딱딱하여 발아율 감소의 원인이 되는 경실률이 환경 및 저장조건에 따라 10∼40%나 된다. 따라서 헤어리베치의 종자 발아율을 증진하기 위하여 침수처리, 종피파상 및 황산처리가 발아에 미치는 영향 조사한 결과 다음과 같다. 헤어리베치 종자를 증류수에 1∼9시간까지 침지 시킨 후 발아율을 조사한 결과 5시간 침지조건에서 초기발아가 가장 좋았으며 발아율에는 큰 차이는 보이지 않았지만 무침지에 비하여 9% 높은 것으로 나타났다. 온도 조건에 따른 발아율의 차이는 83.0∼85.7%로 큰 차이는 없었지만 초기 발아 속도는 10℃의 5%에 비하여 20℃ 31.7%, 30℃ 48.3%로 발아율의 증가를 보였다. 종피파상 (칼집처리) 시험 시 무처리 헤어리베치 종자의 발아율은 65%였고 파상처리 종자의 발아율은 97%로 헤어리베치 종피의 파상처리는 종자의 발아율을 상승시키는데 효과가 큰 것으로 나타났다. 헤어리베치 종자를 10분, 20분 동안 황산처리된 종자의 발아율은 각각 76.7%, 74.7%를 보였으며 30분 동안 처리된 종자는 96.0%의 발아율로 가장 높았다. Seed coat of hairy vetch is very thick and hard, and difficult to absorb water during germination. It requires much time that cotyledon comes out from seed coat. Therefore this experiment was carried out to increase the germination rate by enhancing water absorption through water-soaking of seed, chemical scarification by sulfuric acid, and mechanical scarification on seed coat. Water-soaking for 5 hours seemed to be highly effective in enhancing germination rate. Although not significant, water-soaking resulted in increase of germination rate by 9%. Effect of soaking temperature was not significant, but early germination rate was increased to be 5.0%, 31.7% and 48.3% at 10℃, 20℃ and 30℃, respectively. Mechanical scarification of seed coat led to a germination rate of 97% whereas intact seed showed that of 65%. Chemical scarification by sulfuric acid for 10min, 20min and 30min resulted in a germination rate of 76.7%, 74.7% and 96.0% respectively. It is clear that scarification increased germination rate.
Kim, Min-Ju,Park, Hana,Choi, Seo-Hyeon,Kong, Min-Jeong,Kim, Ji-Eun,Kang, Tae-Cheon MDPI AG 2019 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.20 No.19
<P>2-Cyano-3,12-dioxo-oleana-1,9(11)-dien-28-oic acid methyl ester (CDDO-Me) is a triterpenoid analogue of oleanolic acid that has anti-inflammatory, antioxidant, and neuroprotective activities. In the present study, we evaluate the effects of CDDO-Me on serum extravasation and astroglial death in the rat piriform cortex (PC) induced by status epilepticus (a prolonged seizure activity, SE) in order to propose an underlying pharmacological mechanism of CDDO-Me and its availability for treatment of vasogenic edema. CDDO-Me effectively mitigated serum extravasation and a massive astroglial loss in the PC following SE. CDDO-Me abrogated tumor necrosis factor-α (TNF-α) synthesis in activated microglia by inhibiting nuclear factor-κB (NF-κB) p65 serine 276 phosphorylation. CDDO-Me also abolished NF-κB threonine 435 phosphorylation in endothelial cells and TNF-α-mediated-phosphatidylinositol-3-kinase (PI3K)/AKT/endothelial nitric oxide synthase (eNOS) signaling cascades, which trigger vasogenic edema following SE. Furthermore, CDDO-Me increased astroglial viability via the up-regulation of nuclear factor-erythroid 2-related factor 2 (Nrf2) expression. Therefore, our findings suggest that CDDO-Me may ameliorate SE-induced vasogenic edema formation by regulating NF-κB p65 phosphorylations in microglia as well as endothelial cells and enhancing Nrf2 expression in astrocytes, respectively.</P>
Lee, Jeong-Min,Lee, Jong-Min,Kim, Ki-Ryeong,Im, Hana,Kim, Yang-Hee Elsevier 2015 Biochemical and biophysical research communication Vol.459 No.2
<P><B>Abstract</B></P> <P>During brain ischemic preconditioning (PC), mild bursts of ischemia render neurons resistant to subsequent strong ischemic injuries. Previously, we reported that zinc plays a key role in PC-induced neuroprotection <I>in vitro</I> and <I>in vivo</I>. Zinc-triggered p75<SUP>NTR</SUP> induction transiently activates caspase-3, which cleaves poly(ADP-ribose) polymerase-1 (PARP-1). Subsequently, the PARP-1 over-activation-induced depletion of nicotinamide adenine dinucleotide (NAD<SUP>+</SUP>)/adenosine triphosphate (ATP) after exposures to lethal doses of zinc or N-methyl-<SMALL>D</SMALL>-aspartate is significantly attenuated in cortical neuronal cultures. In the present study, zinc-mediated preconditioning (Zn PC) reduced apoptotic neuronal death that was caused by N,N,N′,N′-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN), etoposide, or staurosporine in mouse cortical cells. We focused on heat shock protein 70 (HSP70) because NAD<SUP>+</SUP>/ATP depletion does not directly cause apoptosis, and HSP70 can inhibit the activation of caspase-9 or caspase-3 by preventing apoptosome formation or cytochrome C release. Zn PC-mediated HSP70 induction was required for neuroprotection against neuronal apoptosis, and geldanamycin-induced HSP70 induction sufficiently blocked neuronal apoptotic cell death. Furthermore, Zn PC-mediated HSP70 induction was blocked by chemical inhibitors of extracellular signal-regulated kinase (ERK) or p38 mitogen-activated protein kinase (MAPK) signaling, but not c-Jun N-terminal protein kinase. Similarly, neuroprotection by Zn PC against TPEN-induced apoptosis was almost completely reversed by the blockade of ERK or p38 MAPK signaling. Our findings suggest that the ERK- or p38 MAPK-mediated induction of HSP70 plays a key role in inhibiting caspase-3 activation during Zn PC.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Pre-incubation with a sublethal concentration of zinc attenuates neuronal apoptosis. </LI> <LI> HSP70 induction is essential for zinc preconditioning-mediated neuroprotection. </LI> <LI> ERK and p38 MAPK, but not JNK, contribute to HSP70-mediated neuroprotection. </LI> </UL> </P>