• Journal of Microbiology and Biotechnology
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• 제34권6호
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• pp.1328-1339
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• 2024

Cadmium (Cd) is a prevalent environmental contaminant that poses a potential hazard to the health of both humans and animals. In this study, biosynthesized selenium-enriched Lactobacillus plantarum and selenium nanoparticles (SeNPs) were developed and evaluated for their protective effects against Cd-induced hepatic injury in mice through oral administration for 4 weeks. Cadmium exposure resulted in severe impairment of liver function, as evidenced by increased levels of serum markers of liver injury and, oxidative stress and significant damage to liver tissue, and a notable decrease in the diversity of the intestinal microbiota. Oral administration of Se-enriched L. plantarum (LS) reduced cadmium accumulation in the liver by 49.5% and, restored other cadmium-induced damage markers to normal levels. A comparison of the effects with those of L. plantarum (L) and SeNPs isolated from LS revealed that LS could more effectively alleviate hepatic oxidative stress and reduce the intrahepatic inflammatory responses of the liver, further protecting against cadmium-induced liver injury. These findings suggest that the development of LS may be effective at protecting the liver and intestinal tract from cadmium-induced damage.

• Tuberculosis and Respiratory Diseases
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• 제65권6호
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• pp.464-470
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• 2008

연구배경: 산소독에 의한 급성 폐손상에 대한 기전은 아직 확실히 알려져 있지 않다. 급성호흡곤란증후군에서 보이는 호중구의 산소기 생성에 따른 조직의 손상이 산소독에 의한 손상에서도 관여하는지를 확인하고자 하였다. 방 법: Plastic cage 내의 기압을 1기압으로 고정하고 흰쥐에게 순수한 산소를 48시간 호흡시킨 후 호중구가 폐장 내로 침윤함으로써 나타나는 급성 폐손상을 생화학적인 지표 및 형태학적인 관찰 등을 통하여 검사하였다. 결 과: 흰쥐에게 순수한 산소를 48시간 호흡하게 한 경우 폐부종, 호중구의 침윤, 폐장 내 MDA 및 $cPLA_2$ 활동도의 증가가 관찰되었고, 형태학적으로도 탐식구 특히 호중구의 침윤에 따른 폐장의 손상이 관찰되었다. 결 론: 산소독에 의한 급성폐손상의 기전은 고농도의 산소에 의한 산소기 생성이 그 원인으로 생각 되지만 산소기의 작용기전은 부분적으로 $cPLA_2$활성도 증가에 의한 호중구의 조직 내 침윤에 따른 이차적 산소기 형성이 그 원인으로 생각되며 시간이 경과할수록 호중구에 폐장 내 침윤에 따른 손상이 더 심해질 것으로 생각된다.

• 한국약용작물학회지
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• 제19권1호
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• pp.31-37
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• 2011

Previous work demonstrated that an ethanol extract (HS0608) of a mixture of three medicinal plants of Curcuma longae radix, Phellinus linteus, and Scutellariae radix markedly inhibits $A{\beta}$ (25-35)-induced neurotoxicity. The present study was performed to further verify the neuroprotective effect of HS0608 on oxidative and ischemic cerebral injury using cultured rat cortical neurons and rats. Exposure of cultured cortical neurons to $100\;{\mu}M$ hydrogen peroxide ($H_2O_2$) induced neuronal apoptotic death. At $10-100{\mu}g/ml$, HS0608 inhibited neuronal death, elevation of intracellular calcium concentration ($[Ca^{2+}]_i$), and generation of reactive oxygen species (ROS) induced by $H_2O_2$ in primary cultures of rat cortical neurons. In vivo, HS0608 prevented cerebral ischemic injury induced by 2-h middle cerebral artery occlusion (MCAO) and 24-h reperfusion. The ischemic infarct and edema were significantly reduced in rats that received HS0608 (200 mg/kg). These results suggest that the anti-oxidative properties of HS0608 may be responsible for its neuroprotective effect against focal cerebral ischemic injury and that HS0608 may have a therapeutic role in neurodegenerative diseases such as stroke.

• 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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• 제23권1호
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• pp.57-64
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• 2002

Objective : This study was designed to investigate the anti-oxidative effects of Oldenlandiae Diffusae Herba Water extract (ODHW) on lipid peroxidation by free radicals oxidative hepatic injury. Methods : In order to evaluate anti-oxidative activities of ODHW in the liver cell, cultured normal rat liver cells(Ac2F) were incubated with or without ODHW. After 16 hours to 18 hours of experiment, cells were placed in DMEM medium without serum, and then incubated with 1mM tert-butyl hydro-peroxide(t-BHP) for two hours. Viable cells were detected by MTT assay. The levels of LPO induced by hydroxyl radical derived from H2O2-Fe2+ system in rat liver homogenate were determined by means of TBA. Inhibitory effect of ODHW on superoxide generation was measured by xanthine-xanthine oxidase system. Results : In the linoleic acid autoxidation system, ODHW exhibited antioxidant activity, which inhibited 85% of linoleic acid peroxidation. These effects were similar to those of dl-a-tocopherol. ODHW showed scavenging effects on DPPH radical, inhibited superoxide generation in xanthine-xanthine oxidase system, and also inhibited lipid peroxidation of rat liver tissue with hydroxyl radical derived from $H_2O_2-Fe^{2+}$ system. In addition, ODHW protected the cell death induced by t-BHP and it significantly increased cell viability in a normal rat liver cell(Ac2F)

• Advances in Traditional Medicine
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• 제9권4호
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• pp.292-302
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• 2009

Ischemia/reperfusion injury, which is commonly seen in the field of renal surgery or transplantation, is a major cause of acute renal failure. Previous studies showed that antioxidant treatments attenuated renal ischemia/reperfusion injury. The objective of this study was to examine the role of hesperidin in modulating reactive oxygen species induced inflammation and apoptosis after renal ischemia/reperfusion injury. Rats were subjected to right nephrectomy, 15 days later 45 min of renal ischemia and 24 h reperfusion with or without treatment with hesperidin. Renal function, inflammation and apoptosis were compared at 24 h after reperfusion injury. Hesperidin improved the renal dysfunction and reduced inflammation and apoptosis after ischemia/reperfusion injury. In conclusion, hesperidin shows potent anti-apoptotic and antiinflammatory properties due to antioxidant property. These findings may have major implications in the treatment of human ischemic acute renal failure.

• Natural Product Sciences
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• 제14권4호
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• pp.244-248
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• 2008

It is well known that excessive production of reactive oxygen species (ROS) leads to oxidative stress, loss of cell function, and ultimately apoptosis or necrosis. To search for natural antioxidants able to modulate cellular oxidative stress, we investigated the protective effect of ethanol extracts of 17 medicinal plants selected from the preliminary antioxidant screening on tert-butyl hydroperoxide (t-BuOOH)-induced oxidative stress in human keratinocytes. The result showed that extracts of the four plants, Distylium racemosum, Astilbe chinensis, Cercis chinensis and Sapium japonicum, exhibited significant cytoprotective activity (over 50% protection) against t-BuOOH-induced cellular injury.

• Journal of Veterinary Science
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• 제24권1호
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• pp.2.1-2.14
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• 2023

Background: Hypothermia is a crucial environmental factor that elevates the risk of cardiovascular disease, but the underlying effect is unclear. Objectives: This study examined the role of cold stress (CS) in cardiac injury and its underlying mechanisms. Methods: In this study, a chronic CS-induced myocardial injury model was used; mice were subjected to chronic CS (4℃) for three hours per day for three weeks. Results: CS could result in myocardial injury by inducing the levels of heat shock proteins 70 (HSP70), enhancing the generation of creatine phosphokinase-isoenzyme (CKMB) and malondialdehyde (MDA), increasing the contents of tumor necrosis factor-α (TNF-α), high mobility group box 1 (HMGB1) interleukin1b (IL-1β), IL-18, IL-6, and triggering the depletion of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). Multiple signaling pathways were activated by cold exposure, including pyroptosis-associated NOD-like receptor 3 (NLRP3)-regulated caspase-1-dependent/Gasdermin D (GSDMD), inflammation-related toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)-mediated nuclear factor kappa B (NF-κB), and mitogen-activated protein kinase (MAPK), as well as oxidative stressinvolved thioredoxin-1/thioredoxin-interacting protein (Txnip) signaling pathways, which play a pivotal role in myocardial injury resulting from hypothermia. Conclusions: These findings provide new insights into the increased risk of cardiovascular disease at extremely low temperatures.

• Biomolecules & Therapeutics
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• 제24권1호
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• pp.33-39
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• 2016

Oxidative stress activates several intracellular signaling cascades that may have deleterious effects on neuronal cell survival. Thus, controlling oxidative stress has been suggested as an important strategy for prevention and/or treatment of neurodegenerative diseases. In this study, we found that ginsenoside Rh1 inhibited hydrogen peroxide-induced reactive oxygen species generation and subsequent cell death in rat primary astrocytes. Rh1 increased the expression of phase II antioxidant enzymes, such as heme oxygenase-1 (HO-1), NAD(P)H:quinone oxidoreductase 1, superoxide dismutase-2, and catalase, that are under the control of Nrf2/ARE signaling pathways. Further mechanistic studies showed that Rh1 increased the nuclear translocation and DNA binding of Nrf2 and c-Jun to the antioxidant response element (ARE), and increased the ARE-mediated transcription activities in rat primary astrocytes. Analysis of signaling pathways revealed that MAP kinases are important in HO-1 expression, and act by modulating ARE-mediated transcriptional activity. Therefore, the upregulation of antioxidant enzymes by Rh1 may provide preventive therapeutic potential for various neurodegenerative diseases that are associated with oxidative stress.

• 생약학회지
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• 제42권3호
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• pp.276-281
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• 2011

Oxidative stress or the accumulation of reactive oxygen species (ROS) leads neuronal cellular death and dysfunction, and it contributes to neuronal degenerative disease such as Alzheimer's disease, Parkinson's disease and stroke. Glutamate-induced oxidative injury contributes to neuronal degeneration in many central nervous system (CNS) diseases, such as epilepsy and ischemia. Heme oxygenase-1 (HO-1) enzyme plays an important role of cellular antioxidant system against oxidant injury. The expression of HO-1 has cytoprotective effects in glutamate-induced oxidative cytotoxicity in HT22 cells. The induction of HO-1 is primarily regulated at the transcriptional level, and its induction by various inducers is related to the nuclear transcription factor-E2-related factor 2 (Nrf2). Nrf2 is a master regulator of the antioxidant response. NNMBS008, the water-insoluble fraction of the 70% EtOH extract of roots of Sophora flavescens, showed dominant neuroprotective effects on glutamate-induced neurotoxicity in mouse hippocampal HT22 cells by induced the expression of HO-1 and increased HO activity. In mouse hippocampal HT22 cells, NNMBS008 makes the nuclear accumulation of Nrf2 pathway. In conclusion, the waterinsoluble fraction of the 70% EtOH extract of roots of S. flavescens (NNMBS008) significantly protect glutamate-induced oxidative damage by induction of HO-1 via Nrf2 pathway in mouse hippocampal HT22 cells. These results suggest that these extracts could be the effective candidates for the treatment of ROS-related neurological diseases.