Intraperitoneal administration of thioredoxin decreases brain damage from ischemic stroke

Intraperitoneal administration of thioredoxin decreases brain damage from ischemic stroke Recent studies demonstrate that Thioredixin (Trx) possesses a neuronal protective effect and closely relates to oxidative stress and apoptosis of cerebral ischemia injury. The present study was conducted to validate the neuroprotective effect of recombinant human Trx-1 (rhTrx-1) and its potential mechanisms against ischemia injury at middle cerebral artery occlusion (MCAO) in mice. rhTrx-1 was administrated intraperitoneally at a dose of 5, 10 and 20mg/kg 30min before MCAO in mice, and its neuronal protective effect was evaluated by neurological deficit score, brain dry–wet weight, 2,3,5-triphenyltetrazolium chloride (TTC) staining. The protein carbonyl content and HO-1 were detected to investigate its potential anti-oxidative and anti-inflammatory property, and the anti-apoptotic ability of rhTrx-1 was assessed by casepase-3 and TUNEL staining. The results demonstrated that rhTrx-1 significantly improved neurological functions and reduced cerebral infarction and apoptotic cell death at 24h after MCAO. Moreover, rhTrx-1 resulted in a significant decrease in carbonyl contents and HO-1 against oxidative stress, which turned to be fast reduction during the first 24h and tended to be stable from 24h to 72h after MCAO. The study shows that rhTrx-1 exerts an neuroprotective effect in cerebral ischemia injury. The anti-oxidative, anti-apoptotic and anti-inflammatory properties of rhTrx-1 are more likely to succeed as a therapeutic approach to diminish oxidative stress-induced neuronal apoptotic cell death in acute ischemic stroke. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Brain Research Elsevier

Intraperitoneal administration of thioredoxin decreases brain damage from ischemic stroke

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Publisher
Elsevier
Copyright
Copyright © 2015 Elsevier B.V.
ISSN
0006-8993
D.O.I.
10.1016/j.brainres.2015.04.033
Publisher site
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Abstract

Recent studies demonstrate that Thioredixin (Trx) possesses a neuronal protective effect and closely relates to oxidative stress and apoptosis of cerebral ischemia injury. The present study was conducted to validate the neuroprotective effect of recombinant human Trx-1 (rhTrx-1) and its potential mechanisms against ischemia injury at middle cerebral artery occlusion (MCAO) in mice. rhTrx-1 was administrated intraperitoneally at a dose of 5, 10 and 20mg/kg 30min before MCAO in mice, and its neuronal protective effect was evaluated by neurological deficit score, brain dry–wet weight, 2,3,5-triphenyltetrazolium chloride (TTC) staining. The protein carbonyl content and HO-1 were detected to investigate its potential anti-oxidative and anti-inflammatory property, and the anti-apoptotic ability of rhTrx-1 was assessed by casepase-3 and TUNEL staining. The results demonstrated that rhTrx-1 significantly improved neurological functions and reduced cerebral infarction and apoptotic cell death at 24h after MCAO. Moreover, rhTrx-1 resulted in a significant decrease in carbonyl contents and HO-1 against oxidative stress, which turned to be fast reduction during the first 24h and tended to be stable from 24h to 72h after MCAO. The study shows that rhTrx-1 exerts an neuroprotective effect in cerebral ischemia injury. The anti-oxidative, anti-apoptotic and anti-inflammatory properties of rhTrx-1 are more likely to succeed as a therapeutic approach to diminish oxidative stress-induced neuronal apoptotic cell death in acute ischemic stroke.

Journal

Brain ResearchElsevier

Published: Jul 30, 2015

References

  • Anti-apoptotic and neuroprotective effects of edaravone following transient focal ischemia in rats
    Amemiya, S.; Kamiya, T.; Nito, C.; Inaba, T.; Kato, K.; Ueda, M.; Shimazaki, K.; Katayama, Y.
  • Oxygen radicals in focal cerebral ischemia
    Chan, P.H.
  • Thioredoxin, a singlet oxygen quencher and hydroxyl radical scavenger: redox independent functions
    Das, K.C.; Das, C.K.
  • Postischemic infusion of Cu/Zn superoxide dismutase or SOD:Tet451 reduces cerebral infarction following focal ischemia/reperfusion in rats
    Francis, J.W.; Ren, J.; Warren, L.; Brown, R.H.; Finklestein, S.P.
  • Thioredoxin and glutaredoxin systems
    Holmgren, A.
  • Thioredoxin-1 attenuates post-ischemic neuronal apoptosis via reducing oxidative/nitrative stress
    Ma, Y.H.; Su, N.; Chao, X.D.; Zhang, Y.Q.; Zhang, L.; Han, F.; Luo, P.; Fei, Z.; Qu, Y.
  • Oxidative stress and neuronal death/survival signaling in cerebral ischemia
    Saito, A.; Maier, C.M.; Narasimhan, P.; Nishi, T.; Song, Y.S.; Yu, F.; Liu, J.; Lee, Y.S.; Nito, C.; Kamada, H.; Dodd, R.L.; Hsieh, L.B.; Hassid, B.; Kim, E.E.; Gonzalez, M.; Chan, P.H.
  • Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1
    Saitoh, M.; Nishitoh, H.; Fujii, M.; Takeda, K.; Tobiume, K.; Sawada, Y.; Kawabata, M.; Miyazono, K.; Ichijo, H.
  • Attenuation of neuronal degeneration in thioredoxin-1 overexpressing mice after mild focal ischemia
    Zhou, F.; Gomi, M.; Fujimoto, M.; Hayase, M.; Marumo, T.; Masutani, H.; Yodoi, J.; Hashimoto, N.; Nozaki, K.; Takagi, Y.

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