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Proper heat shock pretreatment reduces acute liver injury induced by carbon tetrachloride and accelerates liver repair in mice.

Li SQ, Wang DM, Shu YJ, Wan XD, Xu ZS, Li EZ - J Toxicol Pathol (2013)

Bottom Line: Whether proper heat shock preconditioning can reduce liver injury and accelerate liver repair after acute liver injury is worth study.Our results showed that heat shock preconditioning at 40°C for 20 min remarkably improved the mice's survival rate (P<0.05), lowered the levels of serum AST and ALT (P<0.05), induced HSP70 (P<0.01), CYP1A2 (P<0.01) and PCNA (P<0.05) expression, effectively reduced liver injury (P<0.05) and accelerated the liver repair (P<0.05) compared with heat shock preconditioning at 40°C for 10 min or 30 min in the mice after acute liver injury induced by CCl4 when compared with the control mice.Our results may be helpful in further investigation of heat shock pretreatment as a potential clinical approach to target liver injury.

View Article: PubMed Central - PubMed

Affiliation: Molecular Medicine Key Laboratory of Liver Injury and Repair, Medical College, Henan University of Science and Technology, An hui road 31, Jian xi district, Luoyang 471003, P.R. China.

ABSTRACT
Whether proper heat shock preconditioning can reduce liver injury and accelerate liver repair after acute liver injury is worth study. So mice received heat shock preconditioning at 40°C for 10 minutes (min), 20 min or 30 min and recovered at room temperature for 8 hours (h) under normal feeding conditions. Then acute liver injury was induced in the heat shock-pretreated mice and unheated control mice by intraperitoneal (i.p.) injection of carbon tetrachloride (CCl4). Hematoxylin and eosin (H&E) staining, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels and the expression levels of heat shock protein 70 (HSP70), cytochrome P450 1A2 (CYP1A2) and proliferating cell nuclear antigen (PCNA) were detected in the unheated control mice and heat shock-pretreated mice after CCl4 administration. Our results showed that heat shock preconditioning at 40°C for 20 min remarkably improved the mice's survival rate (P<0.05), lowered the levels of serum AST and ALT (P<0.05), induced HSP70 (P<0.01), CYP1A2 (P<0.01) and PCNA (P<0.05) expression, effectively reduced liver injury (P<0.05) and accelerated the liver repair (P<0.05) compared with heat shock preconditioning at 40°C for 10 min or 30 min in the mice after acute liver injury induced by CCl4 when compared with the control mice. Our results may be helpful in further investigation of heat shock pretreatment as a potential clinical approach to target liver injury.

No MeSH data available.


Related in: MedlinePlus

Photomicrographs of immunohistochemical staining of CYP1A2 in the liver of unheated control mice and heat shock-pretreated mice at 0 h after CCl4 administration. The arrowheads indicate the CYP1A2-positive cells in the liver of mice in the control group (A), HS10 group (B), HS20 group (C) and HS30 group (D). E: Numbers of CYP1A2 + cells in the liver of mice in the control group and preheated groups; tissue sections that were at least 12 mm2 were counted for each mouse. (Scale bar: 50 µm).
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fig_005: Photomicrographs of immunohistochemical staining of CYP1A2 in the liver of unheated control mice and heat shock-pretreated mice at 0 h after CCl4 administration. The arrowheads indicate the CYP1A2-positive cells in the liver of mice in the control group (A), HS10 group (B), HS20 group (C) and HS30 group (D). E: Numbers of CYP1A2 + cells in the liver of mice in the control group and preheated groups; tissue sections that were at least 12 mm2 were counted for each mouse. (Scale bar: 50 µm).

Mentions: The expression of HSP70, CYP1A2 and PCNA in the liver of unheated control mice and heat shock-pretreated mice after CCl4 administration. The expression of HSP70, CYP1A2 and PCNA was detected by Western blot (A). The protein bands were quantified for HSP70 (B), CYP1A2 (C) and PCNA (D) with the Gel-Pro Analyzer 4.0 software (Media Cybernetics Inc.) (B), and the intensities of the bands were normalized against β-actin. AU represents arbitrary unit. Every experiment was repeated three times. All data were presented as the mean ± standard error of the mean (SEM). ##P<0.01; significant difference when compared with the HS10 and HS30 groups.


Proper heat shock pretreatment reduces acute liver injury induced by carbon tetrachloride and accelerates liver repair in mice.

Li SQ, Wang DM, Shu YJ, Wan XD, Xu ZS, Li EZ - J Toxicol Pathol (2013)

Photomicrographs of immunohistochemical staining of CYP1A2 in the liver of unheated control mice and heat shock-pretreated mice at 0 h after CCl4 administration. The arrowheads indicate the CYP1A2-positive cells in the liver of mice in the control group (A), HS10 group (B), HS20 group (C) and HS30 group (D). E: Numbers of CYP1A2 + cells in the liver of mice in the control group and preheated groups; tissue sections that were at least 12 mm2 were counted for each mouse. (Scale bar: 50 µm).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3921919&req=5

fig_005: Photomicrographs of immunohistochemical staining of CYP1A2 in the liver of unheated control mice and heat shock-pretreated mice at 0 h after CCl4 administration. The arrowheads indicate the CYP1A2-positive cells in the liver of mice in the control group (A), HS10 group (B), HS20 group (C) and HS30 group (D). E: Numbers of CYP1A2 + cells in the liver of mice in the control group and preheated groups; tissue sections that were at least 12 mm2 were counted for each mouse. (Scale bar: 50 µm).
Mentions: The expression of HSP70, CYP1A2 and PCNA in the liver of unheated control mice and heat shock-pretreated mice after CCl4 administration. The expression of HSP70, CYP1A2 and PCNA was detected by Western blot (A). The protein bands were quantified for HSP70 (B), CYP1A2 (C) and PCNA (D) with the Gel-Pro Analyzer 4.0 software (Media Cybernetics Inc.) (B), and the intensities of the bands were normalized against β-actin. AU represents arbitrary unit. Every experiment was repeated three times. All data were presented as the mean ± standard error of the mean (SEM). ##P<0.01; significant difference when compared with the HS10 and HS30 groups.

Bottom Line: Whether proper heat shock preconditioning can reduce liver injury and accelerate liver repair after acute liver injury is worth study.Our results showed that heat shock preconditioning at 40°C for 20 min remarkably improved the mice's survival rate (P<0.05), lowered the levels of serum AST and ALT (P<0.05), induced HSP70 (P<0.01), CYP1A2 (P<0.01) and PCNA (P<0.05) expression, effectively reduced liver injury (P<0.05) and accelerated the liver repair (P<0.05) compared with heat shock preconditioning at 40°C for 10 min or 30 min in the mice after acute liver injury induced by CCl4 when compared with the control mice.Our results may be helpful in further investigation of heat shock pretreatment as a potential clinical approach to target liver injury.

View Article: PubMed Central - PubMed

Affiliation: Molecular Medicine Key Laboratory of Liver Injury and Repair, Medical College, Henan University of Science and Technology, An hui road 31, Jian xi district, Luoyang 471003, P.R. China.

ABSTRACT
Whether proper heat shock preconditioning can reduce liver injury and accelerate liver repair after acute liver injury is worth study. So mice received heat shock preconditioning at 40°C for 10 minutes (min), 20 min or 30 min and recovered at room temperature for 8 hours (h) under normal feeding conditions. Then acute liver injury was induced in the heat shock-pretreated mice and unheated control mice by intraperitoneal (i.p.) injection of carbon tetrachloride (CCl4). Hematoxylin and eosin (H&E) staining, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels and the expression levels of heat shock protein 70 (HSP70), cytochrome P450 1A2 (CYP1A2) and proliferating cell nuclear antigen (PCNA) were detected in the unheated control mice and heat shock-pretreated mice after CCl4 administration. Our results showed that heat shock preconditioning at 40°C for 20 min remarkably improved the mice's survival rate (P<0.05), lowered the levels of serum AST and ALT (P<0.05), induced HSP70 (P<0.01), CYP1A2 (P<0.01) and PCNA (P<0.05) expression, effectively reduced liver injury (P<0.05) and accelerated the liver repair (P<0.05) compared with heat shock preconditioning at 40°C for 10 min or 30 min in the mice after acute liver injury induced by CCl4 when compared with the control mice. Our results may be helpful in further investigation of heat shock pretreatment as a potential clinical approach to target liver injury.

No MeSH data available.


Related in: MedlinePlus