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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

Serum AST (A) and ALT (B) levels in the mice of the control and pretreatment groups at 0, 3, 6, 12, 24, 30, 36, 42, 48 and 54 h after administration of 0.1 ml/10 g 0.1% CCl4 (1 μl CCl4 in 1 ml mineral oil). Data are expressed as means ± SEM (n=9). HS10 group, HS20 group and HS30 group: mice received heat shock preconditioning with 40°C for 10, 20 and 30 min, respectively and then recovered at room temperature for 8 h under normal feeding conditions; 0.1% CCl4 was subsequently administered to the mice. Control group: mice were only administered 0.1% CCl4. * P<0.05; ** P<0.01; significant difference in the HS group as compared with the control group. # P<0.05 when compared with the HS10 and HS30 groups.
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fig_001: Serum AST (A) and ALT (B) levels in the mice of the control and pretreatment groups at 0, 3, 6, 12, 24, 30, 36, 42, 48 and 54 h after administration of 0.1 ml/10 g 0.1% CCl4 (1 μl CCl4 in 1 ml mineral oil). Data are expressed as means ± SEM (n=9). HS10 group, HS20 group and HS30 group: mice received heat shock preconditioning with 40°C for 10, 20 and 30 min, respectively and then recovered at room temperature for 8 h under normal feeding conditions; 0.1% CCl4 was subsequently administered to the mice. Control group: mice were only administered 0.1% CCl4. * P<0.05; ** P<0.01; significant difference in the HS group as compared with the control group. # P<0.05 when compared with the HS10 and HS30 groups.

Mentions: Figure 1Fig. 1.


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)

Serum AST (A) and ALT (B) levels in the mice of the control and pretreatment groups at 0, 3, 6, 12, 24, 30, 36, 42, 48 and 54 h after administration of 0.1 ml/10 g 0.1% CCl4 (1 μl CCl4 in 1 ml mineral oil). Data are expressed as means ± SEM (n=9). HS10 group, HS20 group and HS30 group: mice received heat shock preconditioning with 40°C for 10, 20 and 30 min, respectively and then recovered at room temperature for 8 h under normal feeding conditions; 0.1% CCl4 was subsequently administered to the mice. Control group: mice were only administered 0.1% CCl4. * P<0.05; ** P<0.01; significant difference in the HS group as compared with the control group. # P<0.05 when compared with the HS10 and HS30 groups.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig_001: Serum AST (A) and ALT (B) levels in the mice of the control and pretreatment groups at 0, 3, 6, 12, 24, 30, 36, 42, 48 and 54 h after administration of 0.1 ml/10 g 0.1% CCl4 (1 μl CCl4 in 1 ml mineral oil). Data are expressed as means ± SEM (n=9). HS10 group, HS20 group and HS30 group: mice received heat shock preconditioning with 40°C for 10, 20 and 30 min, respectively and then recovered at room temperature for 8 h under normal feeding conditions; 0.1% CCl4 was subsequently administered to the mice. Control group: mice were only administered 0.1% CCl4. * P<0.05; ** P<0.01; significant difference in the HS group as compared with the control group. # P<0.05 when compared with the HS10 and HS30 groups.
Mentions: Figure 1Fig. 1.

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