FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2808034659> ?p ?o ?g. }

• W2808034659 abstract "The present study aimed to investigate whether ginsenoside Rb1 (G‑Rb1) attenuates spinal cord injury‑associated oxidative stress in rats by regulating the endothelial nitric oxide synthase eNOS/nuclear factor erythroid 2‑related factor 2 (Nrf2)/heme oxygenase (HO)‑1 signaling pathway. Sprague Dawley rats were randomly divided into the sham operation group (S group), spinal cord injury group (SCI group), G‑Rb1 treatment group (G‑Rb1 group) and SCI+G‑Rb1+Inhibitor L‑name group (L‑name group). The posterior limb function was evaluated via the Basso, Beattie and Bresnahan scoring method. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT) and glutathione (GSH) in serum were measured by ELISA. The pathological changes in the spinal cord were observed by H&E staining. Reverse transcription‑quantitative polymerase chain reaction and western blot analyses were used to detect eNOS, phosphorylated (p)‑eNOS, heat shock protein (HSP)90, Nrf2 and NAD(P)H quinone dehydrogenase 1 (Nqo1) at the mRNA and protein level. Immunohistochemistry was used to detect the expression of Nrf2 and p‑eNOS. Compared with the S group, the scores of spinal cord function in the SCI group were significantly lower, and the levels of MDA were significantly increased, while the levels of SOD, CAT and GSH protein in spinal cord were significantly decreased (P<0.05). The spinal cord tissue exhibited hemorrhage, neuronal degeneration/necrosis, as well as mononuclear cell and lymphocyte infiltration. The eNOS, HSP90, Nrf2, Nqo1 and HO‑1 mRNA levels were decreased (P<0.05). Compared with those in the SCI group, the spinal cord function score in the G‑Rb1 group were significantly higher and the serum MDA content was significantly decreased, while the activity of SOD, CAT and GSH was significantly increased (P<0.05). The degeneration/necrosis of spinal cord neurons was attenuated, inflammatory cell infiltration was significantly reduced and the levels of eNOS, HSP90, Nrf2, Nqo1 and HO‑1 were significantly upregulated (P<0.05). In the group that was administered the eNOS inhibitor L‑name, the levels of eNOS, HSP90, Nrf2, Nqo1 and HO‑1 were significantly decreased. In conclusion, G‑Rb1 attenuates oxidative stress in injured spinal cords. The mechanism may at least in part involve the eNOS/Nrf2/HO‑1 pathway." @default.
• W2808034659 created "2018-06-21" @default.
• W2808034659 creator A5016293805 @default.
• W2808034659 creator A5024125336 @default.
• W2808034659 creator A5038949882 @default.
• W2808034659 creator A5072596159 @default.
• W2808034659 creator A5073170329 @default.
• W2808034659 creator A5078424130 @default.
• W2808034659 creator A5079594267 @default.
• W2808034659 creator A5090731919 @default.
• W2808034659 date "2018-06-12" @default.
• W2808034659 modified "2023-10-16" @default.
• W2808034659 title "Effects of ginsenoside Rb1 on oxidative stress injury in rat spinal cords by regulating the eNOS/Nrf2/HO‑1 signaling pathway" @default.
• W2808034659 cites W1518547765 @default.
• W2808034659 cites W1979929836 @default.
• W2808034659 cites W1980739328 @default.
• W2808034659 cites W1986082290 @default.
• W2808034659 cites W2006617411 @default.
• W2808034659 cites W2019058725 @default.
• W2808034659 cites W2024703353 @default.
• W2808034659 cites W2031869195 @default.
• W2808034659 cites W2033196806 @default.
• W2808034659 cites W2038873703 @default.
• W2808034659 cites W2043462986 @default.
• W2808034659 cites W2054675682 @default.
• W2808034659 cites W2057693298 @default.
• W2808034659 cites W2078628458 @default.
• W2808034659 cites W2094853764 @default.
• W2808034659 cites W2100678791 @default.
• W2808034659 cites W2107277218 @default.
• W2808034659 cites W2111322736 @default.
• W2808034659 cites W2156563278 @default.
• W2808034659 cites W2170645579 @default.
• W2808034659 cites W2192080449 @default.
• W2808034659 cites W2196457931 @default.
• W2808034659 cites W2211557888 @default.
• W2808034659 cites W2480155173 @default.
• W2808034659 cites W2504833408 @default.
• W2808034659 cites W2509189455 @default.
• W2808034659 cites W2510445733 @default.
• W2808034659 cites W2511935072 @default.
• W2808034659 cites W2512913023 @default.
• W2808034659 cites W2523580758 @default.
• W2808034659 cites W2614240925 @default.
• W2808034659 cites W2751535768 @default.
• W2808034659 cites W2770358036 @default.
• W2808034659 cites W50981894 @default.
• W2808034659 doi "https://doi.org/10.3892/etm.2018.6286" @default.
• W2808034659 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6090283" @default.
• W2808034659 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30116359" @default.
• W2808034659 hasPublicationYear "2018" @default.
• W2808034659 type Work @default.
• W2808034659 sameAs 2808034659 @default.
• W2808034659 citedByCount "26" @default.
• W2808034659 countsByYear W28080346592018 @default.
• W2808034659 countsByYear W28080346592019 @default.
• W2808034659 countsByYear W28080346592020 @default.
• W2808034659 countsByYear W28080346592021 @default.
• W2808034659 countsByYear W28080346592022 @default.
• W2808034659 countsByYear W28080346592023 @default.
• W2808034659 crossrefType "journal-article" @default.
• W2808034659 hasAuthorship W2808034659A5016293805 @default.
• W2808034659 hasAuthorship W2808034659A5024125336 @default.
• W2808034659 hasAuthorship W2808034659A5038949882 @default.
• W2808034659 hasAuthorship W2808034659A5072596159 @default.
• W2808034659 hasAuthorship W2808034659A5073170329 @default.
• W2808034659 hasAuthorship W2808034659A5078424130 @default.
• W2808034659 hasAuthorship W2808034659A5079594267 @default.
• W2808034659 hasAuthorship W2808034659A5090731919 @default.
• W2808034659 hasBestOaLocation W28080346591 @default.
• W2808034659 hasConcept C126322002 @default.
• W2808034659 hasConcept C134018914 @default.
• W2808034659 hasConcept C169760540 @default.
• W2808034659 hasConcept C181199279 @default.
• W2808034659 hasConcept C185592680 @default.
• W2808034659 hasConcept C2775838275 @default.
• W2808034659 hasConcept C2776151105 @default.
• W2808034659 hasConcept C2777622882 @default.
• W2808034659 hasConcept C2778326061 @default.
• W2808034659 hasConcept C2778401633 @default.
• W2808034659 hasConcept C2778760513 @default.
• W2808034659 hasConcept C2780775167 @default.
• W2808034659 hasConcept C519581460 @default.
• W2808034659 hasConcept C538909803 @default.
• W2808034659 hasConcept C55493867 @default.
• W2808034659 hasConcept C71924100 @default.
• W2808034659 hasConcept C86803240 @default.
• W2808034659 hasConceptScore W2808034659C126322002 @default.
• W2808034659 hasConceptScore W2808034659C134018914 @default.
• W2808034659 hasConceptScore W2808034659C169760540 @default.
• W2808034659 hasConceptScore W2808034659C181199279 @default.
• W2808034659 hasConceptScore W2808034659C185592680 @default.
• W2808034659 hasConceptScore W2808034659C2775838275 @default.
• W2808034659 hasConceptScore W2808034659C2776151105 @default.
• W2808034659 hasConceptScore W2808034659C2777622882 @default.
• W2808034659 hasConceptScore W2808034659C2778326061 @default.
• W2808034659 hasConceptScore W2808034659C2778401633 @default.
• W2808034659 hasConceptScore W2808034659C2778760513 @default.
• W2808034659 hasConceptScore W2808034659C2780775167 @default.
• W2808034659 hasConceptScore W2808034659C519581460 @default.

• next