Protective effect of doxorubicin induced heat shock protein 72 on cold preservation injury of rat livers

Abstract

AIM:To observe the protective effect of heat shock protein 72 (HSP 72) induced by pretreatment of doxorubicin (DXR) on long-term cold preservation injury of rat livers. METHODS:Sprague-Dawley rats were administered intravenously DXR at a dose of 1 mg/kg body mass in DXR group and saline in control group. After 48 h, the rat liver was perfused with cold Linger's and University of Wisconsin (UW) solutions and then was preserved in UW solution at 4 for 24, 36 and 48 h. AST, ALT, LDH and hyaluronic acid in preservative solution were determined. Routine HE, immunohistochemical staining for HSP 72 and electron microscopic examination of hepatic tissues were performed. RESULTS:After 24, 36 and 48 h, the levels of AST, ALT and hyaluronic acid in preservative solution were significantly higher in control group than in DXR group (P<0.05), while LDH level was not significantly different between the 2 groups (P>0.05). Hepatic tissues in DXR group were morphologically normal and significantly injured in control group. HSP 72 was expressed in hepatocytes and sinusoidal endothelial cells in DXR group but not in control group.CONCLUSION: Pretreatment of DXR may extend the time of rat liver cold preservation and keep liver alive. The expression of HSP 72 in liver can prevent hepatocytes and sinusoidal endothelial cells from long-term cold preservation injury.

Biochemical effects of spirulina platensis against oxidative stress caused by doxorubicin

“…Data represented in Table (1) revealed that activities of serum AST, ALT were markedly elevated in doxorubicin treated groups compared to control group, indicating liver injury. The present results are in agreement with many authors as (Chen et al, 2004) who reported that, doxorubicin treated rats induce significant increases in ALT, AST and bilirubin serum levels when compared with the untreated control group.…”

Modified Mild Heat Shock Modality Attenuates Hepatic Ischemia/Reperfusion Injury

“…But it is still unclear what pathways are involved in the cytokine reduction. One possibility is that the protection of hepatocytes and sinusoidal endothelial cells by Hsp72 prevents microcirculatory failure and, subsequently, the immune cell accumulation [1,33]. However, we cannot rule out the possibility that HS þ MES might have some direct function of suppressing the cytokine expressions.…”

Do Liposomal Apoptotic Enhancers Increase Tumor Coagulation and End-Point Survival in Percutaneous Radiofrequency Ablation of Tumors in a Rat Tumor Model?

“…Indeed, investigators in several studies (15)(16)(17)(18) have demonstrated complementary interactions when they combined RF ablation and concurrent administration of the chemotherapeutic agent doxorubicin, particularly in the form of a liposomal preparation. Researchers in mechanistic studies (19)(20)(21) have further shown that liposomal doxorubicin increases effectiveness of ablation, in part by cellular stress leading to apoptosis, but also produces heat-shock proteins (HSPs), such as 70-kDa HSP (HSP70), which have been shown to limit tissue damage. Therefore, other compounds that have greater apoptosis potential and/or HSP suppression hold the potential to further increase RF ablation-induced tissue coagulation.…”