Limits...
Ischemic postconditioning prevents renal ischemia reperfusion injury through the induction of heat shock proteins in rats.

Guo Q, Du X, Zhao Y, Zhang D, Yue L, Wang Z - Mol Med Rep (2014)

Bottom Line: IR also increased lipid peroxidation, as indicated by elevated malondialdehyde content, reduced superoxide dismutase activity and increased renal apoptosis.Quercetin treatment abolished all the protective effects of IPo.In conclusion, this study showed that IPo can attenuate lipid peroxidation, apoptosis and inflammation as well as renal IRI by upregulating the expression of HSP70, HSP27 and HO‑1.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.

ABSTRACT
Ischemic postconditioning (IPo) attenuates ischemia‑reperfusion injuries (IRI) in various organs, of both animals and humans. This study tested the hypothesis that IPo attenuates renal IRI through the upregulation of heat shock protein (HSP)70, HSP27 and heme oxygenase‑1 (HO‑1, also known as HSP 32) expression. Adult Sprague Dawley rats were subjected to bilateral renal ischemia for 45 min followed by reperfusion for up to 48 h. One group of rats received IPo prior to restoring full perfusion. Another group was administered 100 mg/kg HSP inhibitor quercetin, injected intraperitoneally 1 h prior to ischemia. Control rats received sham operations. Renal IR resulted in severe morphological and pathological changes, with increased serum creatinine and blood urea nitrogen concentrations. IR resulted in increased inflammation by inducing plasma tumor necrosis factor‑α and renal nuclear factor kappa‑light‑chain‑enhancer of activated B cells expression. IR also increased lipid peroxidation, as indicated by elevated malondialdehyde content, reduced superoxide dismutase activity and increased renal apoptosis. Renal HSP70, HSP27 and HO‑1 mRNA and protein levels were increased by IR and further elevated by IPo. IPo attenuated these changes observed in pathology, lipid peroxidation, apoptosis and inflammation. Quercetin treatment abolished all the protective effects of IPo. In conclusion, this study showed that IPo can attenuate lipid peroxidation, apoptosis and inflammation as well as renal IRI by upregulating the expression of HSP70, HSP27 and HO‑1.

Show MeSH

Related in: MedlinePlus

Microphotographs of kidney tissues in the four experimental groups at 6 h post-reperfusion (hematoxylin and eosin stain; magnification, ×400). (A) Control group showed no obvious morphological changes. (B) Ischemia-reperfusion group showed severe pathological and morphological changes, tubular dilatation, cellular edema, with partly visible necrosis and tubular cells. Protein accumulation was detected in the fluid within lumen, together with perivascular dilatation and congestion. (C) The IPo group showed an attenuation of the pathological changes. (D) Quercetin + IPo attenutated the renoprotective effects of IPo. IPo, ischemic postconditioning.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4227421&req=5

f2-mmr-10-06-2875: Microphotographs of kidney tissues in the four experimental groups at 6 h post-reperfusion (hematoxylin and eosin stain; magnification, ×400). (A) Control group showed no obvious morphological changes. (B) Ischemia-reperfusion group showed severe pathological and morphological changes, tubular dilatation, cellular edema, with partly visible necrosis and tubular cells. Protein accumulation was detected in the fluid within lumen, together with perivascular dilatation and congestion. (C) The IPo group showed an attenuation of the pathological changes. (D) Quercetin + IPo attenutated the renoprotective effects of IPo. IPo, ischemic postconditioning.

Mentions: To assess functional renal impairment, changes in renal pathology were observed by microscopy, and levels of Cr and BUN were measured in the serum. Renal IR led to severe pathological and morphological changes, including tubular dilatation and cellular edema, with partly visible necrosis and tubular cells. Protein accumulation in the fluid within lumen, perivascular dilatation and congestion (Fig. 2) as well as increased serum Cr expression levels (102±5 vs. 46±6 μmol/l, P<0.05) and BUN (25.7±3.9 vs. 5.1±1.9 mmol/l, P<0.05) concentrations at 6 h after reperfusion were also observed. IPo attenuated the pathological changes and decreased Cr expression levels (64±5 vs. 102±5 μmol/l, P<0.05) and BUN concentrations (11.3±3.0 vs. 25.7±3.9 mmol/l, P<0.05) (Fig. 3A and B). The renoprotective effects of IPo were significantly attenuated by quercetin (Cr, 101±6 vs. 64±5 μmol/l, P<0.05; BUN, 26.5±4.5 vs. 11.3±3.0, P<0.05).


Ischemic postconditioning prevents renal ischemia reperfusion injury through the induction of heat shock proteins in rats.

Guo Q, Du X, Zhao Y, Zhang D, Yue L, Wang Z - Mol Med Rep (2014)

Microphotographs of kidney tissues in the four experimental groups at 6 h post-reperfusion (hematoxylin and eosin stain; magnification, ×400). (A) Control group showed no obvious morphological changes. (B) Ischemia-reperfusion group showed severe pathological and morphological changes, tubular dilatation, cellular edema, with partly visible necrosis and tubular cells. Protein accumulation was detected in the fluid within lumen, together with perivascular dilatation and congestion. (C) The IPo group showed an attenuation of the pathological changes. (D) Quercetin + IPo attenutated the renoprotective effects of IPo. IPo, ischemic postconditioning.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4227421&req=5

f2-mmr-10-06-2875: Microphotographs of kidney tissues in the four experimental groups at 6 h post-reperfusion (hematoxylin and eosin stain; magnification, ×400). (A) Control group showed no obvious morphological changes. (B) Ischemia-reperfusion group showed severe pathological and morphological changes, tubular dilatation, cellular edema, with partly visible necrosis and tubular cells. Protein accumulation was detected in the fluid within lumen, together with perivascular dilatation and congestion. (C) The IPo group showed an attenuation of the pathological changes. (D) Quercetin + IPo attenutated the renoprotective effects of IPo. IPo, ischemic postconditioning.
Mentions: To assess functional renal impairment, changes in renal pathology were observed by microscopy, and levels of Cr and BUN were measured in the serum. Renal IR led to severe pathological and morphological changes, including tubular dilatation and cellular edema, with partly visible necrosis and tubular cells. Protein accumulation in the fluid within lumen, perivascular dilatation and congestion (Fig. 2) as well as increased serum Cr expression levels (102±5 vs. 46±6 μmol/l, P<0.05) and BUN (25.7±3.9 vs. 5.1±1.9 mmol/l, P<0.05) concentrations at 6 h after reperfusion were also observed. IPo attenuated the pathological changes and decreased Cr expression levels (64±5 vs. 102±5 μmol/l, P<0.05) and BUN concentrations (11.3±3.0 vs. 25.7±3.9 mmol/l, P<0.05) (Fig. 3A and B). The renoprotective effects of IPo were significantly attenuated by quercetin (Cr, 101±6 vs. 64±5 μmol/l, P<0.05; BUN, 26.5±4.5 vs. 11.3±3.0, P<0.05).

Bottom Line: IR also increased lipid peroxidation, as indicated by elevated malondialdehyde content, reduced superoxide dismutase activity and increased renal apoptosis.Quercetin treatment abolished all the protective effects of IPo.In conclusion, this study showed that IPo can attenuate lipid peroxidation, apoptosis and inflammation as well as renal IRI by upregulating the expression of HSP70, HSP27 and HO‑1.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.

ABSTRACT
Ischemic postconditioning (IPo) attenuates ischemia‑reperfusion injuries (IRI) in various organs, of both animals and humans. This study tested the hypothesis that IPo attenuates renal IRI through the upregulation of heat shock protein (HSP)70, HSP27 and heme oxygenase‑1 (HO‑1, also known as HSP 32) expression. Adult Sprague Dawley rats were subjected to bilateral renal ischemia for 45 min followed by reperfusion for up to 48 h. One group of rats received IPo prior to restoring full perfusion. Another group was administered 100 mg/kg HSP inhibitor quercetin, injected intraperitoneally 1 h prior to ischemia. Control rats received sham operations. Renal IR resulted in severe morphological and pathological changes, with increased serum creatinine and blood urea nitrogen concentrations. IR resulted in increased inflammation by inducing plasma tumor necrosis factor‑α and renal nuclear factor kappa‑light‑chain‑enhancer of activated B cells expression. IR also increased lipid peroxidation, as indicated by elevated malondialdehyde content, reduced superoxide dismutase activity and increased renal apoptosis. Renal HSP70, HSP27 and HO‑1 mRNA and protein levels were increased by IR and further elevated by IPo. IPo attenuated these changes observed in pathology, lipid peroxidation, apoptosis and inflammation. Quercetin treatment abolished all the protective effects of IPo. In conclusion, this study showed that IPo can attenuate lipid peroxidation, apoptosis and inflammation as well as renal IRI by upregulating the expression of HSP70, HSP27 and HO‑1.

Show MeSH
Related in: MedlinePlus