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Journal of Zhejiang University SCIENCE B 2005 Vol.6 No.1 P.28~32

http://doi.org/10.1631/jzus.2005.B0028


Effects of β-Aescin on the expression of nuclear factor-κB and tumor necrosis factor-α after traumatic brain injury in rats


Author(s):  XIAO Guo-min, WEI Jing

Affiliation(s):  Department of Neurosurgery, Hangzhou Second Hospital, Hangzhou 310015, China

Corresponding email(s):   xgm@zjedu.org

Key Words:  Brain injuries, &beta, -Aescin, Nuclear factor-&kappa, B, Tumor necrosis factor-&alpha


XIAO Guo-min, WEI Jing. Effects of β-Aescin on the expression of nuclear factor-κB and tumor necrosis factor-α after traumatic brain injury in rats[J]. Journal of Zhejiang University Science B, 2005, 6(1): 28~32.

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author="XIAO Guo-min, WEI Jing",
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volume="6",
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pages="28~32",
year="2005",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.2005.B0028"
}

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%T Effects of β-Aescin on the expression of nuclear factor-κB and tumor necrosis factor-α after traumatic brain injury in rats
%A XIAO Guo-min
%A WEI Jing
%J Journal of Zhejiang University SCIENCE B
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%N 1
%P 28~32
%@ 1673-1581
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%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.2005.B0028

TY - JOUR
T1 - Effects of β-Aescin on the expression of nuclear factor-κB and tumor necrosis factor-α after traumatic brain injury in rats
A1 - XIAO Guo-min
A1 - WEI Jing
J0 - Journal of Zhejiang University Science B
VL - 6
IS - 1
SP - 28
EP - 32
%@ 1673-1581
Y1 - 2005
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.2005.B0028


Abstract: 
To investigate the inhibiting effect of beta%29&ck%5b%5D=abstract&ck%5b%5D=keyword'>b>&beta;b%5D=abstract&ck%5b%5D=keyword'>b>-Aescin on b%5D=abstract&ck%5b%5D=keyword'>b>nuclear factor-&kappa;b (NF-κb) activation and the expression of tumor necrosis factor-&alpha; (TNF-α) protein after traumatic brain injury (TbI) in the rat brain, 62 SD rats were subjected to lateral cortical impact injury caused by a free-falling object and divided randomly into four groups: (1) sham operated (Group A); (2) injured (Group b); (3) beta%29&ck%5b%5D=abstract&ck%5b%5D=keyword'>b>&beta;b%5D=abstract&ck%5b%5D=keyword'>b>-Aescin treatment (Group C); (4) pyrrolidine dithocarbamate (PDTC) treatment (Group D). beta%29&ck%5b%5D=abstract&ck%5b%5D=keyword'>b>&beta;b%5D=abstract&ck%5b%5D=keyword'>b>-Aescin was administered in Group C and PDTC treated in Group D immediately after injury. A series of brain samples were obtained directly 6 h, 24 h and 3 d respectively after trauma in four groups. NF-κb activation was examined by Electrophoretic Mobility Shift Assay (EMSA); the levels of TNF-α protein were measured by radio-immunoassay (RIA); the water content of rat brain was measured and pathomorphological observation was carried out. NF-κb activation, the levels of TNF-α protein and the water content of rat brain were significantly increased (P<0.01) following TbI in rats. Compared with Group b, NF-κb activation (P<0.01), the levels of TNF-α protein (P<0.01) and the water content of brain (P<0.05) began to decrease obviously after injury in Groups C and D. beta%29&ck%5b%5D=abstract&ck%5b%5D=keyword'>b>&beta;b%5D=abstract&ck%5b%5D=keyword'>b>-Aescin could dramatically inhibit NF-κb activation and the expression of TNF-α protein in the rat brain, alleviate rat brain edema, and that could partially be the molecular mechanism by which beta%29&ck%5b%5D=abstract&ck%5b%5D=keyword'>b>&beta;b%5D=abstract&ck%5b%5D=keyword'>b>-Aescin attenuates traumatic brain edema.

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Reference

[1] Baeuerle, P., Baltimore, D., 1996. NF-kappa B: Ten years after. Cell, 87:13-20.

[2] Bakdwin, A.S.Jr., 1996. The NF-κB and IκB proteins: new discoveries and insights. Annu Rev Immunol, 14:649-683.

[3] Beg, A.A., Bakdwin, A.S.Jr., 1993. The IκB proteins: multifunctional regulators of Rel/NF-κB transcription factors. Gene Dev, 9:427-433.

[4] Beg, A.A., Ruben, S.M., Schcinman, R.I., Haskill, S., Rosen, C.A., Baldwin, A.S.Jr., 1992. I kappa B interacts with the nuclear localization sequences of the subunits of NF-κB: a mechanism for cytoplasmic retention. Genes Dev, 10:1899-1913.

[5] Connor, T.J., Song, C., Leonard, B.E., Anisman, H., Merali, Z., 1998. An assessment of the effects of central interleukin-1 beta, -2, -6, and tumor necrosis factor-alpha administration on some behavioural neurochemical, endocrine and immune paramenters in the rat. Neuroscience, 84:923-933.

[6] Fransserr, C., Defraigne, J.O., Detry, O., 1995. Antioxidant defense and free radical production in a rabbit model of kidney ischemia-reperfusion. Transplant-Proc, 27:2880-2883.

[7] Hiai, S., Yokoyama, H., Oura, H., 1981. Effect of Aescin of adreno-corticotropin and corticosterone levels in rat plasma. Chen Pharm Bull, 29:490.

[8] Ichikawa, K., DeGroot, L.J., Refetoff, S.H., Nuorwitz, A.L., Pollak, E.R., 1986. Nuclear thyroid hormone receptors in cultured human fibrobasts: improved method of isolation, partial characterization, and interaction with chromation. Metabolism, 35:861-868.

[9] Korner, M., Rattner, A., Mauxion, F., Sen, R., Citri, Y., 1989. A brain specific transcription activator. Neuron, 3:563-572.

[10] Lee, J.I., Burekart, G.J., 1988. Nuclear factor-kappa B: important transcription factor and therapeatic target. J Clin Pharmacol, 38:981-993.

[11] Lü, H.S., 1993. (-Aescin and appliation in clinic. J Tongji Medical University, 22(3):218-220 (in Chinese).

[12] Nanaka, M., Chen, X.H., Pierce, J.E., Leoni, M.J., MeIntosk, T.K., Wolf, J.A., Smith, D.H., 1999. Prolonged activation of NF-κB following traumatic brain injury in rats. J Neurotrauma, 16:1023-1034.

[13] Stover, J.F., Schoning, B., Sakowitz, O.W., Woiciechowsky, C., Unterberg, A.W., 2001. Effects of tacrolimus on hemispheric water content and cerebrospinal fluid levels of glutamate, hypoxanthine, interleukin-6, and tumor necrosis actor-alpha following controlled cortical impact injury in rats. J Neurosurg, 94:782-787.

[14] Sullivan, P.G., Bruce-Keller, A.J., Rabchevsky, A.G., Chrislakos, S., Clair, D.K., Mattson, M.P., Scheff, S.W., 1999. Exacerbation of damage and altered NF-κB activation in mice lacking tumor necrosis factor receptors after traumatic brain injury. J Neurosci, 19:6248-3260.

[15] Suzumura, A., Ito, A., Yoshikowa, M., Sawada, M., 1999. Ibudilast suppresses TNF alpha production by glial cells functioning mainly as type III phosphodiesterast inhibition in the CNS. Brain Res, 837:203-212.

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