• Biotechnology and Bioprocess Engineering:BBE
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• 제8권6호
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• pp.322-330
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• 2003

The unicellular green alga Haematococcus pluvialis has recently attracted great inter-est due to its large amounts of ketocarotenoid astaxanthin, 3,3'-dihydroxy-${\beta}$,${\beta}$-carotene-4,4'-dione, widely used commercially as a source of pigment for aquaculture. In the life cycle of H. pluvialis, astaxanthin biosynthesis is associated with a remarkable morphological change from green motile vegetative cells into red immotile cyst cells as the resting stage. In recent years we have studied this morphological process from two aspects: defining conditions governing astaxanthin biosynthesis and questioning the possible function of astaxanthin in protecting algal cells against environmental stress. Astaxanthin accumulation in cysts was induced by a variety of environmental conditions of oxidative stress caused by reactive oxygen species, intense light, drought, high salinity, and high temperature. In the adaptation to stress, abscisic acid induced by reactive oxygen species, would function as a hormone in algal morphogenesis from veget ative to cyst cells. Furthermore, measurements of both in vitro and in vivo antioxidative activities of astaxanthin clearly demonstrated that tolerance to excessive reactive oxygen species is greater in astaxanthin-rich cysts than in astaxanthin-poor cysts or astaxanthin-less vegetative cells. Therefore, reactive oxygen species are involved in the regulation of both algal morph O-genesis and carotenogenesis, and the accumulated astaxanthin in cysts can function as a protective agent against oxidative stress damage. In this study, the physiological roles of astaxanthin in stress response and cell protection are reviewed.

• 대한한의학회지
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• 제30권2호
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• pp.88-103
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• 2009

Objectives: There is currently increased interest in the identification of natural antioxidant compounds derived from various plants. Peony Root (PR) is used worldwide for the treatment of many types of cardiovascular disease including atherosclerosis and hypertension. It has been used in Korean traditional medicine for the treatment of glycosuria, hypertension and cancer. However, to date, no studies concerning the antioxidant properties of PR have been conducted. Therefore, this study was conducted to evaluate the in vitro scavenging activity, inhibitory effect of LDL oxidation of pro-oxidant reactive species and anti-thrombosis effect in response to treatment with PR using various screening methods including biological and non-biological oxidants. Methods: In this study, the antioxidant activity of extract from PR was studied with in vitro methods by measuring the antioxidant activity by TEAC, measuring the scavenging effects on reactive oxygen species (ROS) [superoxide anion, hydroxyl radical] and on reactive nitrogen species (RNS) [nitric oxide and peroxynitrite] as well as measuring the inhibitory effect on $Cu^{2+}$-induced human LDL oxidation and the inhibitory effect on collagen-induced platelet aggregation. Results: The PR extracts were found to have a potent scavenging activity of oxidative stress [DPPH, superoxide anion, hydroxyl radical, nitric oxide and peroxynitrite, etc.] as well as an inhibitory effect on LDL oxidation and on platelet aggregation. Conclusions: The PR extracts have anti-oxidative and anti-atherosclerotic effects in vitro system, which can be used for developing pharmaceutical drugs against oxidative stress and atherosclerosis.

• 대한한의학회지
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• 제37권2호
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• pp.62-75
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• 2016

Objectives: This study examined whether Lycii Radicis Cortex has an inhibitory effect on inflammatory response through an oxidative stress and advanced glycation endproducts (AGEs)-mediated pathway in streptozotocin (STZ)-induced type 1 diabetic rats. Methods: Lycii Radicis Cortex was orally administered to STZ-induced diabetic rats in doses of 80 or 160 mg/kg body weight/day for 2 weeks, and its effects were compared with those of diabetic control and normal rats. Results: The administration of Lycii Radicis Cortex decreased the elevated serum urea nitrogen and renal reactive oxygen species (ROS), and reduced the increased AGEs in the serum and kidney. The elevated protein expressions of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits in the kidney of diabetic control rats were significantly decreased after Lycii Radicis Cortex treatments. Moreover, the kidney of diabetic rats exhibited the up-regulation of receptor for AGEs (RAGE) and AGEs-related proteins; however, Lycii Radicis Cortex treatment also significantly reduced those expressions (excepted RAGE). In addition, the diabetic rats exhibited an up-regulation of the expression of proteins related to inflammation in the kidney, but Lycii Radicis Cortex administration reduced significantly the expression of the inflammatory proteins through the nuclear factor-kappa B (NF-${\kappa}B$) and activator protein-1 (AP-1) pathways. Conclusions: This study provides scientific evidence that Lycii Radicis Cortex exerts the antidiabetic effect by inhibiting the expressions of AGEs and NF-${\kappa}B$ in the STZ-induced diabetic rats.

• Toxicological Research
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• 제31권1호
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• pp.49-59
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• 2015

Eye is a highly vascularised organ. There are chances that a foreign substance can enter the systemic circulation through the eye and cause oxidative stress and evoke immune response. Here the eyes of rabbits were exposed, for a period of 7 days, to 5 known ocular irritants: Cetyl pyridinium chloride (CPC), sodium salicylate (SS), imidazole (IMI), acetaminophen (ACT) and nicotinamide (NIC). The eyes were scored according to the draize scoring. Blood collected from the treated rabbit were analyzed for haematological and biochemical parameters. After sacrifice, histological analysis of the eye and analysis of pro-inflammatory biomarkers ($IL-1{\alpha}$, $IL-1{\beta}$, IL-8 and $TNF-{\alpha}$) in the cornea using ELISA was carried out. Spleen was collected and the proliferation capacities of spleenocytes were analyzed. Liver and brain were collected and assessed for oxidative stress. The eye irritation potential of the chemicals was evident from the redness and swelling of the conjunctiva and cornea. Histopathological analysis and ELISA assay showed signs of inflammation in the eye. However, the haematological and biochemical parameters showed no change. Spleenocyte proliferations showed only slight alterations which were not significant. Also oxidative stress in the brain and liver were negligible. In conclusion, chemicals which cause ocular irritation and inflammation did not show any systemic side-effects in the present scenario.

• Molecules and Cells
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• 제22권1호
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• pp.51-57
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• 2006

Haloperidol is a classical neuroleptic drug that is still in clinical use and can lead to abnormal motor activity following repeated administration. However, there is little knowledge of how it triggers neuronal impairment. In this study, we report that it induced calcium ion influx via L-type calcium channels and that the elevation of calcium ions induced by haloperidol appeared to render hippocampal cells more susceptible to oxidative stress. Indeed, the level of cytotoxic reactive oxygen species (ROS) and the expression of pro-apoptotic Bax increased in response to oxidative stress in haloperidol-treated cells, and these effects were inhibited by verapamil, a specific L-type calcium channel blocker, but not by the T-type calcium channel blocker, mibefradil. These findings indicate that haloperidol induces calcium ion influx via L-type calcium channels and that this calcium influx influences neuronal fate.

• 한국식품영양과학회지
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• 제35권10호
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• pp.1329-1335
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• 2006

AIDS로의 진행과정은 단순히 몇몇 기작에 의한 것이 아니라 여러 경로를 거쳐 발생하며 그 진행속도도 개개인에 따라 다양하게 나타나고 있다. 본 연구에서는 쥐 AIDS 모델을 이용하여 항산화호르몬으로 알려진 DHEAS의 면역조절 효과를 확인하고자 하였다. DHEAS의 투여는 LP-BM5 retrovirus 감염으로 인한 T와 B 임파구의 mitogenesis를 증가시켰으며 Th1/Th2 type cytokines의 발현에도 영향을 미쳤는데 주로 전사수준에서 작용한 것으로 생각된다/ 또한 retrovirus 감염으로 인한 간조직의 지질과산화 유발을 억제하여 조직 내의 항산화제인 vitamin E의 함량을 유지시킴으로 NF-kB의 활성화를 통한 retrovirus의 복제를 억제시켜 Th1/Th2 type cytokines의 불균형적인 발현을 저해하였을 것으로 여겨진다. 따라서 쥐 AIDS모델에 있어서 DHEAS의 면역조절 효과를 확인한 본 연구는 향후 HIV감염 이후 AIDS로의 진행 과정 시 항산화제의 역할과 기작 규명에 대한 가능성을 제시할 수 있을 것으로 생각된다.

• BMB Reports
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• 제46권7호
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• pp.370-375
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• 2013

Ischemia is characterized by oxidative stress and changes in the antioxidant defense system. Our recent in vitro study showed that 2-cyclopropylimino-3-methyl-1,3-thiazoline hydrochloride protects cortical astrocytes against oxidative stress. In the current study, we examined the effects of 2-cyclopropylimino-3-methyl-1,3-thiazoline hydrochloride on ischemia-induced neuronal damage in a gerbil ischemia/reperfusion models. Extensive neuronal death in the hippocampal CA1 area was observed 4 days after ischemia/reperfusion. Intraperitoneal injection of 2-cyclopropylimino-3-methyl-1,3-thiazoline hydrochloride (0.3 mg/kg body weight) significantly prevented neuronal death in the CA1 region of the hippocampus in response to transient forebrain ischemia. 2-Cyclopropylimino-3-methyl-1,3-thiazoline hydrochloride administration reduced ischemia-induced increases in reactive oxygen species levels and malondialdehyde content. It also attenuated the associated reductions in glutathione level and superoxide dismutase, catalase, and glutathione peroxidase activities. Taken together, our results suggest that 2-cyclopropylimino-3-methyl-1,3-thiazoline hydrochloride protects against ischemia-induced neuronal damage by reducing oxidative stress through its antioxidant actions.

• 한국응용과학기술학회지
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• 제35권4호
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• pp.1369-1378
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• 2018

홍어 껍질 유래 콜라겐 펩타이드를 한외여과막을 이용하여 분자량의 크기를 1,000 Da 이하와 1,000 Da 이상으로 분리하고 그 효과를 비교하고자 하였다. 각각의 시료를 비만 유발 실험동물인 db/db mice에 체중당 200 mg의 콜라겐 펩타이드를 8주간 투여하였다. 본 연구의 결과는 콜라겐 펩타이드를 투여한 군에서 비만대조군에 비해 체중 증가량의 감소, 혈액 및 간조직의 활성산소 농도의 감소, 간조직의 산화적 스트레스가 완화된 것으로 나타났다. 또한 콜라겐 투여군에서 염증반응과 관련된 간조직의 핵전사인자($NF-{\kappa}B$) 및 효소(COX2, iNOS), 염증성 사이토카인(IL-6)발현이 비만대조군에 비해 유의적으로 감소하였다. 분자량의 크기에 따라 약간의 차이가 나타났지만, 전반적으로는 유의적이지 않았다. 따라서 홍어 콜라겐 펩타이드의 비만에 의해 유발된 염증반응이 억제되었는데, 이는 콜라겐의 산화적 스트레스 완화작용에 기인한 것으로 사료된다.

• Biomolecules & Therapeutics
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• 제29권3호
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• pp.311-320
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• 2021

Accumulation of reactive oxygen species (ROS) is associated with the development of various diseases. However, the molecular mechanisms underlying oxidative stress that lead to such diseases like autosomal dominant polycystic kidney disease (ADPKD) remain unclear. Here, we observed that oxidative stress markers were increased in Pkd1f/f:HoxB7-Cre mice. Forkhead transcription factors of the O class (FOXOs) are known key regulators of the oxidative stress response, which have been observed with the expression of FoxO3a in an ADPKD mouse model in the present study. An integrated analysis of two datasets for differentially expressed miRNA, such as miRNA sequencing analysis of Pkd1 conditional knockout mice and microarray analysis of samples from ADPKD patients, showed that miR-132-3p was a key regulator of FOXO3a in ADPKD. miR-132-3p was significantly upregulated in ADPKD which directly targeted FOXO3 in both mouse and human cell lines. Interestingly, the mitochondrial gene Gatm was downregulated in ADPKD which led to a decreased inhibition of Foxo3. Overexpression of miR-132-3p coupled with knockdown of Foxo3 and Gatm increased ROS and accelerated cyst formation in 3D culture. This study reveals a novel mechanism involving miR-132-3p, Foxo3, and Gatm that is associated with the oxidative stress that occurs during cystogenesis in ADPKD.

• 한국동물학회:학술대회논문집
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• 한국동물학회 1998년도 한국생물과학협회 학술발표대회
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• pp.323.1-323
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• 1998

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