• Title/Summary/Keyword: Intermittent long-term heat stress

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Korean Red Ginseng alleviates neuroinflammation and promotes cell survival in the intermittent heat stress-induced rat brain by suppressing oxidative stress via estrogen receptor beta and brain-derived neurotrophic factor upregulation

  • Iqbal, Hamid;Kim, Si-Kwan;Cha, Kyu-Min;Jeong, Min-Sik;Ghosh, Prachetash;Rhee, Dong-kwon
    • Journal of Ginseng Research
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    • v.44 no.4
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    • pp.593-602
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    • 2020
  • Background: Heat stress orchestrates neurodegenerative disorders and results in the formation of reactive oxygen species that leads to cell death. Although the immunomodulatory effects of ginseng are well studied, the mechanism by which ginseng alleviates heat stress in the brain remains elusive. Methods: Rats were exposed to intermittent heat stress for 6 months, and brain samples were examined to elucidate survival and antiinflammatory effect after Korean Red Ginseng (KRG) treatment. Results: Intermittent long-term heat stress (ILTHS) upregulated the expression of cyclooxygenase 2 and inducible nitric oxide synthase, increasing infiltration of inflammatory cells (hematoxylin and eosin staining) and the level of proinflammatory cytokines [tumor necrosis factor α, interferon gamma (IFN-γ), interleukin (IL)-1β, IL-6], leading to cell death (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay) and elevated markers of oxidative stress damage (myeloperoxidase and malondialdehyde), resulting in the downregulation of antiapoptotic markers (Bcl-2 and Bcl-xL) and expression of estrogen receptor beta and brain-derived neurotrophic factor, key factors in regulating neuronal cell survival. In contrast, KRG mitigated ILTHS-induced release of proinflammatory mediators, upregulated the mRNA level of the antiinflammatory cytokine IL-10, and increased myeloperoxidase and malondialdehyde levels. In addition, KRG significantly decreased the expression of the proapoptotic marker (Bax), did not affect caspase-3 expression, but increased the expression of antiapoptotic markers (Bcl-2 and Bcl-xL). Furthermore, KRG significantly activated the expression of both estrogen receptor beta and brain-derived neurotrophic factor. Conclusion: ILTHS induced oxidative stress responses and inflammatory molecules, which can lead to impaired neurogenesis and ultimately neuronal death, whereas, KRG, being the antioxidant, inhibited neuronal damage and increased cell viability.

Long Term Reliability of Fluroelastomer (FKM) O-ring after Exposure to High Pressure Hydrogen Gas

  • Choi, Myung-Chan;Lee, Jin-Hyok;Yoon, Yu-mi;Jeon, Sang-Koo;Bae, Jong-Woo
    • Elastomers and Composites
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    • v.55 no.4
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    • pp.270-276
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    • 2020
  • The long-term durability of an FKM O-ring used as parts of a hydrogen station was investigated by exposing it to high-pressure gaseous hydrogen for 1, 3, and 7 days at room temperature. Changes in its sealing force were subsequently measured at 150℃ using intermittent compression stress relaxation (CSR). No changes in the tensile properties of FKM O-ring were observed, but its initial and overall sealing forces at 150℃ significantly decreased with increasing exposure time to hydrogen gas. Microvoid formation in the FKM O-ring upon exposure to high-pressure hydrogen was minimized over time after the ring was exposed to atmospheric pressure at room temperature, which prevented changes in its tensile properties. However, applying heat accelerated FKM O-ring oxidation, which decreased its sealing force. These results indicated that identifying changes in the sealing force of rubber materials using intermittent CSR is not sufficient for monitoring changes in mechanical properties under high-pressure hydrogen atmospheres; however, it is suitable for evaluating the long-term durability of sealing materials for hydrogen station applications under similar conditions.