• Korean Journal of Acupuncture
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• 제27권2호
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• pp.13-24
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• 2010

Objectives : Ulcerative colitis is a chronic relapsing inflammatory disease in the gastrointestinal tract. We investigated whether Aurantii fructus immaturus (AFI) pharmacopuncture has antioxidative and anti-inflammatory effects. Methods : in vitro experiments, 1,1-diphenyl-2-picryl hydrazyl (DPPH) free radical scavenging activity, superoxide dismutase (SOD) activity, prevention on $H_2O_2$-induced cell death in RAW264.7 cell line, DNA fragmentation, and cyclooxygenase-2 mRNA expression induced by lipopolysaccharide (LPS), were analyzed to investigate antioxidative and anti-inflammatory effect of AFI pharmacopuncture. in vivo experiment, a murine model of dextran sulfate sodium (DSS)-induced colitis was used to examine the effect of AFI pharmacopuncture on CV12 at different doses of 5 ${\mu}l$, 0.5 ${\mu}l$, 0.05 ${\mu}l$ for 10 days. Body weight, colon length and macroscopic features were investigated. Results : AFI pharmacopuncture showed DPPH free radical scavenging and SOD active effects in a dose-dependent manner. AFI pharmacopuncture showed a protective effect against $H_2O_2$-induced cell injury and also attenuated LPS-induced COX-2 mRNA expression. In a DSS- induced colitis murine model, however, AFI pharmacopuncture at CV12 had no anti-inflammatory effects. Conclusions : The present results suggest that AFI pharmacopuncture extract may have anti- inflammatory and antioxidative effects in vivo test, but further research on the underlying mechanism is required.

• 대한치과마취과학회지
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• 제14권1호
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• pp.49-56
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• 2014

Background: Propofol (2.6-diisopropylphenol) is a widely used intravenous anesthetic agent for the induction and maintenance of anesthesia during surgeries and sedation for ICU patients. Propofol has a structural similarity to the endogenous antioxidant vitamin E and exhibits antioxidant activities.13) However, the mechanism of propofol on hypoxia/reoxygenation (H/R) injury has yet to be fully elucidated. We investigated how P-PostC influences the autophagy and cell death, a cellular damage occurring during the H/R injury. Methods: The groups were randomly divided into the following groups: Control: cells were incubated in normoxia (5% CO2, 21% O2, and 74% N2) without propofol treatment. H/R: cells were exposed to 24 h of hypoxia (5% CO2, 1% O2, and 94% N2) followed by 12 h of reoxygenation (5% CO2, 21% O2, and 74% N2). H/R + P-PostC: cells post-treated with propofol were exposed to 24 h of hypoxia followed by 12 h of reoxygenation. 3-MA + P-PostC: cells pretreated with 3-MA and post-treated propofol were exposed to 24 h of hypoxia followed by 12 h of reoxygenation Results: The results of our present study provides a new direction of research on mechanisms of propofol-mediated cytoprotection. There are three principal findings of these studies. First, the application of P-PostC at the onset of reoxygenation after hypoxia significantly increased COS-7 cell viability. Second, the cellular protective effect of P-PostC in H/R induced COS-7 cells was probably related to activation of intra-cellular autophagy. And third, the autophagy pathway inhibitor 3-MA blocked the protective effect of P-PostC on cell viability, suggesting a key role of autophagy in cellular protective effect of P-PostC. Conclusions: These data provided evidence that P-PostC reduced cell death in H/R model of COS-7 cells, which was in agreement with the protection by P-PostC demonstrated in isolated COS-7 cells exposed to H/R injury. Although the this study could not represent the protection by P-PostC in vivo, the data demonstrate another model in which endogenous mechanisms evoked by P-PostC protected the COS-7 cells exposed to H/R injury from cell death.

• 동의생리병리학회지
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• 제20권4호
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• pp.936-941
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• 2006

To prevent human body injury from oxidative stress, antioxidants are very important and many research about antioxidants are generally being conducted. Hydrogen peroxide$(H_20_2)$ that is one of vitality oxygen species has been seen that cause various diseases, DNA damage and gene change. We have already known that the inhibition effect of Zizania latifolia Radix, Rhizoma on apoptosis induced by $H_2O_2$ in Neuro2A cell. And the purpose of this study was that we made a comparative study on the inhibition effect of apoptosis in Neuro2A cell on the region of Zizania latifolia(Radix, Rhizoma, Herba). Neuro2A cells were cultivated in RPMI(GibcoBRL) with 5% FBS and treated with $H_2O_2$ and Zizania latifolia(Radix, Rhizoma, Herba). Separately we measured the cell viability and analyzed DNA fragmentation. Activity of PARP, Cytochrome C, caspase-9, caspase-3, p53, p21, Bax and Bcl-2 in the cell was examined by using western blot. The results obtained were as Follows: The cell viability in all of Zizania latifolia (Radix, Rhizoma, Herba) treatment (60ug/m1<) decreased significantly compared with that of none treatment(p<0.001). Zizania latifolia Radix increased cell viability was most effective of three regions. But we had no significant difference among three regions. All of Zizania latifolia (Radix, Rhizoma, Herba) increased cell viability about twice as much as that being injury by $H_2O_2$,(Zizania Latifolia (Radix, nhizoma, Herba) 20ug/m1, $H_2O_2$ 200uM, p<0.001). DNA fragmentation developed by $H_2O_2$, but was not developed in all of Zizania latifolia (Radix, Rhizoma, Herba) treatment. PARP, Cytochrome C, caspase-9 and caspase-3 activated all by $H_2O_2$ but were not activated in all of Zizania latifolia (Radix, Rhizoma, Herba) treatment. P53, P2l and Bax activated by $H_2O_2$, and Bcl-2 got into inactivation. But the opposite results appeared in all of Zizania latifolia (Radix, Rhizoma, Herba) treatment. In conclusion, these results suggest that all of Zizania latifolia (Radix, Rhizoma, Herba) inhibit the development of DNA fragmentation and apoptosis by $H_2O_2$and the antioridant action of all of Zizania latifolia (Radix, Rhizoma, Herba) is effective.

• The Korean Journal of Physiology and Pharmacology
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• 제20권3호
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• pp.315-324
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• 2016

Human cardiac fibroblasts (HCFs) have various voltage-dependent $K^+$ channels (VDKCs) that can induce apoptosis. Hydrogen peroxide ($H_2O_2$) modulates VDKCs and induces oxidative stress, which is the main contributor to cardiac injury and cardiac remodeling. We investigated whether $H_2O_2$ could modulate VDKCs in HCFs and induce cell injury through this process. In whole-cell mode patch-clamp recordings, application of $H_2O_2$ stimulated $Ca^{2+}-activated$ $K^+$ ($K_{Ca}$) currents but not delayed rectifier $K^+$ or transient outward $K^+$ currents, all of which are VDKCs. $H_2O_2-stimulated$ $K_{Ca}$ currents were blocked by iberiotoxin (IbTX, a large conductance $K_{Ca}$ blocker). The $H_2O_2-stimulating$ effect on large-conductance $K_{Ca}$ ($BK_{Ca}$) currents was also blocked by KT5823 (a protein kinase G inhibitor) and 1 H-[1, 2, 4] oxadiazolo-[4, 3-a] quinoxalin-1-one (ODQ, a soluble guanylate cyclase inhibitor). In addition, 8-bromo-cyclic guanosine 3', 5'-monophosphate (8-Br-cGMP) stimulated $BK_{Ca}$ currents. In contrast, KT5720 and H-89 (protein kinase A inhibitors) did not block the $H_2O_2-stimulating$ effect on $BK_{Ca}$ currents. Using RT-PCR and western blot analysis, three subtypes of $K_{Ca}$ channels were detected in HCFs: $BK_{Ca}$ channels, small-conductance $K_{Ca}$ ($SK_{Ca}$) channels, and intermediate-conductance $K_{Ca}$ ($IK_{Ca}$) channels. In the annexin V/propidium iodide assay, apoptotic changes in HCFs increased in response to $H_2O_2$, but IbTX decreased $H_2O_2$-induced apoptosis. These data suggest that among the VDKCs of HCFs, $H_2O_2$ only enhances $BK_{Ca}$ currents through the protein kinase G pathway but not the protein kinase A pathway, and is involved in cell injury through $BK_{Ca}$ channels.

• The Korean Journal of Physiology and Pharmacology
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• 제24권6호
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• pp.473-479
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• 2020

Endothelial cell injury is a major contributor to cardiovascular diseases. The 2,3,5,4'-Tetrahydroxystilbene-2-O-β-D-Glucoside (TSG) contributes to alleviate human umbilical vein endothelial cells (HUVECs) injury through mechanisms still know a little. This study aims to clarify the TSG effects on gene expression (mRNA and microRNA) related to oxidative stress and endoplasmic reticulum stress induced by H₂O₂ in HUVECs. We found that TSG significantly reduced the death rate of cells and increased intracellular superoxide dismutase activity. At qRT-PCR, experimental data showed that TSG significantly counteracted the expressions of miR-9-5p, miR-16, miR-21, miR-29b, miR-145-5p, and miR-204-5p. Besides, TSG prevented the expression of ATF6 and CHOP increasing. In contrast, TSG promoted the expression of E2F1. In conclusion, our results point to the obvious protective effect of TSG on HUVECs injury induced by H₂O₂, and the mechanism may through miR16/ATF6/ E2F1 signaling pathway.

• 대한한방내과학회지
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• 제22권2호
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• pp.183-191
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• 2001

신경교세포에서 황금추출물이 반응성 산소기에 의한 세포 사망을 방지할 수 있는지를 확인하기 위하여 사람의 glioama 세포주인 A172 세포를 사용하여 $H_2O_2$의 독성작용에 대한 영향을 조사하였다. 세포 사망 정도는 tryptan blue exclusion과 MTT reduction assay로 평가하였다. $H_2O_2$는 세포 사망을 유도하였으며 또한 세포내 ATP 함량을 감소시켰으며, 이러한 효과는 황금 추출물에 의해 방지되었으며 그 효과는 농도 의존적으로 나타났다. $H_2O_2$에 의한 세포 사망은 잘 알려진 flavonoid인 quercetin과 철착염제인 phenanthroline에 의해 방지되었으나, 항산화제인 DPPD나 Trolox에 의해서는 영향을 받지 않았다. $H_2O_2$는 poly (ADP-ribose) polymerase를 활성화시켰으며, 이러한 효과는 황금, quercetin 및 phenanthroline에 의해 억제되었다. 황금 추출물은 유기산화제인 t-buthyhydroperoxide 및 중금속인 수은에 의한 세포 사망을 방지하였다. 이러한 실험 결과는 황금 추출물이 $H_2O_2$에 의한 세포 사망을 방지하며 그 효과는 황금의 flavonoid 성분이 철과 결합하여 $H_2O_2$로부터 hydroxy radical의 생성을 억제함으로써 나타나는 것으로 추측된다.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.143.1-143.1
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• 2003

In this study. we investigated whether the cardioprotective effect shown by quercetin 3-O-$\alpha$-arabinofuranoside extracted from Lindera erythrocarpa against ROS-induced cell death in H9c2 cardiac myocytes. Cell death was induced by BSO, buthionine sulfoximine, which inhibits GSH level and subsequntly increase ROS level. Cell death was quntitatively determined by measuring lactate dehydrogenase (LDH) activity. (omitted)

• 대한한방내과학회지
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• 제32권4호
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• pp.487-496
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• 2011

Objectives : The aim of this study was to investigate the hepatoprotective effect of Soshiho-tang (SSH) in mouse primary liver cells against hydrogen peroxide ($H_2O_2$)-induced oxidative stress. We also elucidated the molecular mechanism of hepatoprotective effect by SSH. Methods : Cell viability, level of ALT, AST and LDH, intracellular ROS level, mRNA expression and activity of antioxidant enzymes were used to evaluate hepatoprotection of SSH against $H_2O_2$. Target gene expressions were analyzed by real-time PCR. Results : Pre-treatment with SSH for 1 hour prevented cytotoxicity against $H_2O_2$. $H_2O_2$-induced ROS level decreased under SSH pre-treatment. mRNA expression of GPx and SOD increased in SSH-treated cells. In addition, HSP72 and HSP40 gene expression were elevated under SSH-treatment. Conclusions : These results indicate that SSH protects mouse primary liver cells from $H_2O_2$-induced oxidative injury. This hepatoprotective activity of SSH is mediated by decreasing intracellular ROS and increasing antioxidant enzyme expression (GPx and SOD) and stress response protein (HSP72 and HSP40).

• Food Science and Biotechnology
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• 제16권6호
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• pp.1035-1040
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• 2007

Epidemiologic studies have shown important relationships between oxidative stress and Alzheimer's disease (AD) brain. In this study, free radical scavenging activity and neuronal cell protection effect of aqueous methanol extracts of Acanthopanax senticosus (A. senticosus) were examined. $H_2O_2$-induced oxidative stress was measured using 2',7'-dichlorofluorescein diacetate (DCF-DA) assay. Pretreatment with the phenolics of A. senticosus prevented oxidative injury against $H_2O_2$ toxicity. Since oxidative stress is known to increase neuronal cell membrane breakdown, leading to cell death, lactic dehydrogenase release, and trypan blue exclusion assays were utilized. We found that phenolics of A. senticosus have neuronal cell protection effects. It suggests that the phenolics of A. senticosus inhibited $H_2O_2$-induced oxidative stress and A. senticosus may be beneficial against the oxidative stress-induced risk in AD.

• Biomolecules & Therapeutics
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• 제25권6호
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• pp.599-608
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• 2017

Tanshinone IIA (Tan IIA) is a pharmacologically active substance extracted from the rhizome of Salvia miltiorrhiza Bunge (also known as the Chinese herb Danshen), and is widely used to treat atherosclerosis. The pregnane X receptor (PXR) is a nuclear receptor that is a key regulator of xenobiotic and endobiotic detoxification. Tan IIA is an efficacious PXR agonist that has a potential protective effect on endothelial injuries induced by xenobiotics and endobiotics via PXR activation. Previously numerous studies have demonstrated the possible effects of Tan IIA on human umbilical vein endothelial cells, but the further mechanism for its exerts the protective effect is not well established. To study the protective effects of Tan IIA against hydrogen peroxide ($H_2O_2$) in human umbilical vein endothelial cells (HUVECs), we pretreated cells with or without different concentrations of Tan IIA for 24 h, then exposed the cells to $400{\mu}M$ $H_2O_2$ for another 3 h. Therefore, our data strongly suggests that Tan IIA may lead to increased regeneration of glutathione (GSH) from the glutathione disulfide (GSSG) produced during the GSH peroxidase-catalyzed decomposition of $H_2O_2$ in HUVECs, and the PXR plays a significant role in this process. Tan IIA may also exert protective effects against $H_2O_2$-induced apoptosis through the mitochondrial apoptosis pathway associated with the participation of PXR. Tan IIA protected HUVECs from inflammatory mediators triggered by $H_2O_2$ via PXR activation. In conclusion, Tan IIA protected HUVECs against $H_2O_2$-induced cell injury through PXR-dependent mechanisms.