• 동의신경정신과학회지
• /
• 제20권2호
• /
• pp.19-29
• /
• 2009

Objectives : Antioxidant effects of Gagam-jangwonhwan(LMK01 and 02) water extract against $H_2O_2$-induced oxidative damage and cell death were investigated in rat pheochromocytoma line PC 12. Methods : The cells were treated with LMK01 and 02 water extract and $H_2O_2$, oxidative damage-inducing materials for 24 h. The cellular viability was assessed by WST-1 assay, oxidative damages of the cells by 8-OHdG quantitation, apoptosis by Hoechst 33342 staining assay and activity of antioxidant enzymes by catalase and glutathione peroxidase assay. Results : 1. LMK01 and LMK02 water extracts improved significantly cell viability in $H_2O_2$-treated groups than $H_2O_2$-alone treated cells 2, LMK02 suppressed significantly oxidative damage in $H_2O_2$-treated groups than $H_2O_2$-alone treated cells but LMK01 didn't. Meanwhile, difference of oxidative damages in conditions treated with LMK01 or LMK02 was not significant, 3. The $H_2O_2$ induced-apoptosis in PC 12 cell lines was inhibited effectively by LMK01 and LMK02, and especially the features of apoptosis were obviously reduced in LMK02-treated cells. 4. LMK01 and LMK02 increased significantly activities of both catalase and glutathione peroxidase than those of $H_2O_2$-alone treated group and moreover, LMK02 showed significantly higher activities than those of LMK01. Conclusions : As shown, LMK01 and LMK02 suppressed $H_2O_2$-induced oxidative damage and cell death in PC 12 cell effectively. And they increased activity of major antioxidant enzymes in PC 12 cell line. Therefore, this study suggests the possibility of clinical usage over oxidative stress-induced neurodegenerative disease such as Alzheimer's disease.

• Environmental Analysis Health and Toxicology
• /
• 제19권4호
• /
• pp.335-344
• /
• 2004

Diesel exhaust particle (<2.5 ${\mu}{\textrm}{m}$, DEP$_{2.5}$) is known to be probarbly carcinogenic (IARC group 2A). DEP$_{2.5}$ contains organic compounds such as polycyclicaromatic hydrocarbon (PAH), heterocyclic compounds, phenols, and nitroarenes. Reactive oxygen species (ROS) are generated by DEP$_{2.5}$ without any biological activation system. Therefore, an alternative mechanism by which DEP$_{2.5}$ could be carcinogenic is known by the generation of oxidative DNA damage. The aim of this study was to investigate genotoxic effects of DEP$_{2.5}$ using single cell gel electrophoresis. In order to evaluate the mechanisms of DEP$_{2.5}$ genotoxicity, the rat micro-some mediated and DNA repair enzyme treated comet assays together with routine comet assay were performed. DEP$_{2.5}$ was collected from diesel engine bus and dichloromethane extract was obtained. The organic extract of DEP$_{2.5}$ revealed DNA damage itself in NIH/3T3 cells. And it showed both oxidative and microsome mediated DNA damages. Vitamin C as an model antioxidant reduced DNA damage in endonuclase III treated comet assay. One of flavonoid, galangin as a CYP1A1 inhibitor reduced DNA damage in the presence of S-9 mixture. Our results show that DEP$_{2.5}$ are genotoxic and a great source of oxidative stress, but antioxidants can significantly reduce oxidative DNA damages. And DEP$_{2.5}$ may contain indirect mutagens which can be inhibited by CYP inhibitors.d by CYP inhibitors.

• BMB Reports
• /
• 제40권6호
• /
• pp.1039-1049
• /
• 2007

Overdoses of acetaminophen cause hepato-renal oxidative stress. The present study was undertaken to investigate the protective effect of a 43 kDa protein isolated from the herb Cajanus indicus, against acetaminophen-induced hepatic and renal toxicity. Male albino mice were treated with the protein for 4 days (intraperitoneally, 2 mg/kg body wt) prior or post to oral administration of acetaminophen (300 mg/kg body wt) for 2 days. Levels of different marker enzymes (namely, glutamate pyruvate transaminase and alkaline phosphatase), creatinine and blood urea nitrogen were measured in the experimental sera. Intracellular reactive oxygen species production and total antioxidant activity were also determined from acetaminophen and protein treated hepatocytes. Indices of different antioxidant enzymes (namely, superoxide dismutase, catalase, glutathione-S-transferase) as well as lipid peroxidation end-products and glutathione were determined in both liver and kidney homogenates. In addition, Cytochrome P450 activity was also measured from liver microsomes. Finally, histopathological studies were performed from liver sections of control, acetaminophen-treated and protein pre- and post-treated (along with acetaminophen) mice. Administration of acetaminophen increased all the serum markers and creatinine levels in mice sera along with the enhancement of hepatic and renal lipid peroxidation. Besides, application of acetaminophen to hepatocytes increased reactive oxygen species production and reduced the total antioxidant activity of the treated hepatocytes. It also reduced the levels of antioxidant enzymes and cellular reserves of glutathione in liver and kidney. In addition, acetaminophen enhanced the cytochrome P450 activity of liver microsomes. Treatment with the protein significantly reversed these changes to almost normal. Apart from these, histopathological changes also revealed the protective nature of the protein against acetaminophen induced necrotic damage of the liver tissues. Results suggest that the protein protects hepatic and renal tissues against oxidative damages and could be used as an effective protector against acetaminophen induced hepato-nephrotoxicity.

• 생명과학회지
• /
• 제17권11호
• /
• pp.1571-1575
• /
• 2007

본 연구는 당뇨병으로 인한 산화적 스트레스에 대한 함박잎새버섯분말의 효과를 밝히기 위하여 SD계 흰쥐를 STZ로 당뇨를 유발하여 간 및 신장 조직에서 조사하였다. 또한 당뇨흰쥐에 함박잎새버섯분말 1-2% 첨가하여 6주간 식이하였다. 산화적 스트레스의 지표물질인 LPO를 비롯하여 유발원 XOD 활성도를 측정하였다. 또한 이에 따른 간조직 손상 확인을 위해 혈청 ALT와 AST 활성도를 측정하였다. 특히 함박잎새버섯분말의 항산화적 효능을 위해 이들 지표물질들과 더불어 항산화체계의 중요 요소인 GSH 농도와 GST 활성도를 당뇨군, 당뇨-잎새버섯분말투여군 그리고 정상군에서 측정하였다. 당뇨군은 정상군과 비교하여 LPO 농도를 비롯하여 XOD 활성도가 유의하게 높았다. 특히 이러한 결과로 추정되는 간 조직 손상이 정상군보다 유의하게 높은 ALT 및 AST 활성도가 혈청에서 확인되었다. 그러나 당뇨-잎새버섯분말투여군에서는 LPO 농도, XOD 활성도를 비롯하여 조직손상의 지표인 ALT 및 AST 활성도가 당뇨군보다 유의하게 감소하였다. 항산화물질인 GSH 농도는 당뇨군 및 당뇨-잎새버섯분말투여군 비교에서 유의한 차이가 없었으나 GST 활성도는 당뇨-잎새버섯분말투여군이 당뇨군보다 유의하게 높았다. 따라서 당뇨유발성 산화적 스트레스에 대한 잎새버섯분말의 효능은 GSH 농도 변화보다 GST 활성도를 증가시키고 또한 산화적 스트레스의 유발원인 XOD 활성도 감소의 유도를 통해 이루어지는 것으로 추정된다. 결론적으로 당뇨는 산화적 스트레스를 증가시키며 조직손상을 유발한다. 그러나 함박잎새버섯분말은 항산화물질 및 효소계의 활성도를 증가시켜 당뇨유발-산화적 스트레스 감소를 유도하여 조직 손상을 감소시키는 것이 확인되었다.

• 한국약용작물학회지
• /
• 제20권4호
• /
• pp.245-250
• /
• 2012

Dieldrin, one of the organochlorine pesticides (OCPs), induced the damages in neuroblastoma cells and DNA damages in lymphocytes. The ethanol extracts of A. sessiliflorus leaves were examined for the suppressive effects on the dieldrin-induced cell damages. Moreover, the extract was used to test whether it might inhibit the oxidative DNA damage of lymphocytes using Comet assay. The cell and DNA damage by dieldrin were suppressed in vitro upon treating A. sessiliflorus extract. This result suggests that A. sessiliflorus extract might be useful to reduce dieldrin toxicity.

• 대한한방내과학회지
• /
• 제26권2호
• /
• pp.420-430
• /
• 2005

The water extract of Omijatang(OMJT) has been traditionally used for treatment of abscess and heart palpitation in oriental medicine, However, little is known about the mechanism by which the water extract of OMJT rescues cells from these damages. This study was designed to investigate the protective mechanisms of OMJT in H9c2 cardiomyoblasts on oxidative stress-induced cytotoxicity including $H_2O_2,\;ZnCl_2$, hypoxia, and reoxygenation. Oxidative stress markedly decreased the viability of H9c2 cells. This was characterized with apparent apoptotic features such as chromatin condensation as well as fragmentation of genomic DNA and nuclei. However, OMJT significantly reduced $H_2O_2$-induced cell death and apoptotic characteristics as well as $ZnCl_2$, hypoxialreoxygenation. Taken together, this study suggests that the water extract of OMJT has the protective effects against oxidative injuries.

• 대한약침학회지
• /
• 제25권4호
• /
• pp.344-353
• /
• 2022

Objectives: Auraptene is the most abundant natural prenyloxycoumarin. Recent studies have shown that it has multiple biological and therapeutic properties, including antioxidant properties. Erythrocytes are constantly subjected to oxidative damage that can affect proteins and lipids within the erythrocyte membrane and lead to some hemoglobinopathies. Due to the lack of sufficient information about the antioxidant effects of auraptene on erythrocytes, this study intended to evaluate the potential of this compound in protecting radical-induced erythrocytes damages. Methods: The antioxidant activity of auraptene was measured based on DPPH and FRAP assays. Notably, oxidative hemolysis of human erythrocytes was used as a model to study the ability of auraptene to protect biological membranes from free radical-induced damage. Also, the effects of auraptene in different concentrations (25-400 µM) on AAPH-induced lipid/protein peroxidation, glutathione (GSH) content and morphological changes of erythrocytes were determined. Results: Oxidative hemolysis and lipid/protein peroxidation of erythrocytes were significantly suppressed by auraptene in a time and concentration-dependent manner. Auraptene prevented the depletion of the cytosolic antioxidant GSH in erythrocytes. Furthermore, it inhibited lipid and protein peroxidation in a time and concentration-dependent manner. Likewise, FESEM results demonstrated that auraptene reduced AAPH-induced morphological changes in erythrocytes. Conclusion: Auraptene efficiently protects human erythrocytes against free radicals. Therefore, it can be a potent candidate for treating oxidative stress-related diseases.

• 대한화장품학회지
• /
• 제30권1호
• /
• pp.39-51
• /
• 2004

Ozone(O$_3$), one of best-known toxic air pollutant, act as a strong oxidant. It is possible that skins exposed to the air can be easily damaged by such oxidative air pollutants. Therefore, in the present study, anti-oxidative effects of natural product. on $O_2$ㆍ and ㆍOH were investigated by EPR. Ozone caused protein damage and lipid oxidation, in HaCaT and B16F10 leading ultimately to programmed cell death. It also reduced the level of antioxidant molecules including ascorbic acid and tocopherol in stratum comeum. However, antioxidants originated from natural products could protect skin from these products could protect skin from these oxidative damages. We concluded that eight natural extracts including Rosa davurica, Ligularia sibrica, Green tea acted as strong antioxidants against ozone.

• International Journal of Industrial Entomology and Biomaterials
• /
• 제28권2호
• /
• pp.85-91
• /
• 2014

This study was designed to find out the effect of Nosema spore on oxidative damages and antioxidant defence in the midgut of tasar silkworm Antheraea mylitta. Higher level of lipid peroxidation (LPX) and total hydroperoxides indicate the resultant oxidative stress in the Nosema exposed specimen. Increased superoxide dismutase (SOD) suggests activation of physiological mechanism to scavenge the superoxide radical produced during Nosema infection. Higher activities of catalase and glutathione-S-tranferase on $18^{th}$ d indicate adaptive behaviour of the tissue against oxyradicals. The results suggest that Nosema infection is involved in altering the active oxygen metabolism by modulating LPX and reactive oxygen species (ROS), which is indicative of pebrine disease disorder.

• 대한본초학회지
• /
• 제28권4호
• /
• pp.57-62
• /
• 2013

Objectives : Lonicerae Japonicae Flos (LJF) has been shown anti-oxidant, anti-inflammatory, anti-viral, anti-rheumatoid properties. However, it is still largely unknown whether LJF inhibits skin injury against oxidative stress in human keratinocyte, HaCaT cells. The purpose of this study was to evaluate the protective effects of LJF against hydrogen peroxide($H_2O_2$)-induced oxidative stress in human keratinocytes, HaCaT cells. Methods : To evaluate out the protective effects of LJF on oxidative injury in HaCaT cells, an oxidative stress model of HaCaT cells was established under a suitable concentration (500 ${\mu}M$) hydrogen peroxide. HaCaT keratinocyte cells were pre-treated with LJF (0.1, 0.25 or 0.5 mg/ml), and then stimulated with $H_2O_2$. Then, the cells were harvested to measure the cell viability, DNA damage, and release of reactive oxygen species (ROS). Results : LJF (0.1, 0.25 or 0.5 mg/ml) itself did not show any significant toxicity in HaCaT cells. The treatment of $H_2O_2$ caused the oxidative stress, leading to the cell death, and DNA injury. However, pretreatment with LJF reduced cell death, and DNA injury. The stimulation of $H_2O_2$ on HaCaT cells resulted in excessive release of ROS, which is the main factor of oxidative stress. The excessive release of ROS was inhibited by LJF treatment significantly. Conclusions : These results could suggest that LJF exhibited the protective effects of HaCaT cells against $H_2O_2$-induced oxidative stress by inhibiting ROS release. It could be explained that LJF inhibit skin damages against oxidative stress. Thus, LJF would be useful for the development of drug or cosmetics treating skin troubles.