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Dexmedetomidine attenuates acute kidney injury induced by hemorrhagic shock/resuscitation in rats / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 680-685, 2018.
Article in Chinese | WPRIM | ID: wpr-701179
ABSTRACT

AIM:

To investigate the effects of dexmedetomidine on hemorrhagic shock /resuscitation(HS/R)-induced acute kidney injury(AKI)in rats,and to explore the possible mechanisms.

METHODS:

Wistar rats(n=32) were randomly divided into 4 groups(n =8) normal saline control group(NS group), dexmedetomidine group(D group),HS/R group and HS/R+D group.The animals were sacrificed at 6 h after resuscitation.The levels of serum creatinine(Cr)and blood urine nitrogen(BUN)were examined.The kidneys of all rats were removed for evaluation of histological characteristics,and the levels of malondialdehyde(MDA),tumor necrosis factor-α(TNF-α),interleukin-1β (IL-1β)and superoxide dismutase(SOD)were measured.The expression of nuclear factor-κB(NF-κB)and hemeoxyge-nase-1(HO-1)was determined by Western blot.

RESULTS:

Compared with NS group, the levels of Cr, BUN, MDA, TNF-αand IL-1βwere obviously increased in HS/R group, which were obviously decreased in HS/R+D group(P<0.05).Compared with NS group,the SOD activity was obviously decreased in HS/R group,which was obviously increased in HS/R+D group(P<0.05).Compared with NS group, the protein expression of NF-κB was obviously increased in HS/R group,which was obviously decreased in HS/R+D group(P<0.05).Compared with NS group, the protein ex-pression of HO-1 was increased in HS/R group.Compared with HS/R group,the protein expression of HO-1 was obviously increased in HS/R+D group.Compared with NS group,HS/R induced marked kidney histological injury,which was less pronounced in HS/R+D group.

CONCLUSION:

Dexmedetomidine effectively protects rats against AKI caused by HS /R, and its mechanism may be associated with the increase in HO-1 expression and the inhibition of NF-κB expression.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2018 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2018 Type: Article