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Role of Exogenous Hsp72 on Liver Dysfunction during Sepsis.

Tsai TN, Ho JJ, Liu MS, Lee TY, Lu MC, Liu CJ, Huang LJ, Lue SI, Yang RC - Biomed Res Int (2015)

Bottom Line: Apoptosis was determined using terminal deoxynucleotidyl transferase dUTP nick end labeling staining.B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), cleaved caspase-3 and caspase-9, and cleaved poly (ADP-ribose) polymerase (PARP) protein expressions were analyzed using Western blotting.The Bcl-2/Bax ratio, cleaved caspase-3, caspase-9, and PARP protein expressions in the liver tissues were upregulated during sepsis and normalized after rhHsp72 treatment.

View Article: PubMed Central - PubMed

Affiliation: Graduate Institute of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.

ABSTRACT
This study examined the role of exogenous heat shock protein 72 (Hsp72) in reversing sepsis-induced liver dysfunction. Sepsis was induced by cecal ligation and puncture. Liver function was determined on the basis of the enzymatic activities of serum glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT). Apoptosis was determined using terminal deoxynucleotidyl transferase dUTP nick end labeling staining. B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), cleaved caspase-3 and caspase-9, and cleaved poly (ADP-ribose) polymerase (PARP) protein expressions were analyzed using Western blotting. Results showed GOT and GPT levels increased during sepsis, and levels were restored following the administration of human recombinant Hsp72 (rhHsp72). Increased liver tissue apoptosis was observed during sepsis, and normal apoptosis resumed on rhHsp72 administration. The Bcl-2/Bax ratio, cleaved caspase-3, caspase-9, and PARP protein expressions in the liver tissues were upregulated during sepsis and normalized after rhHsp72 treatment. We conclude that, during sepsis, exogenous Hsp72 restored liver dysfunction by inhibiting apoptosis via the mitochondria-initiated caspase pathway.

No MeSH data available.


Related in: MedlinePlus

Effects of rhHsp72 on liver function. Serum samples were harvested 18 h after CLP and sham surgery. Liver function was determined through enzymatic analysis of glutamate oxaloacetate transaminase (GOT) (a) and glutamate pyruvate transaminase (GPT) (b). Experiments were conducted as described in Section 2. Values are mean ± standard error of the mean. Each group contained 12 animals. ∗∗p < 0.01 and N.S. versus sham.
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fig1: Effects of rhHsp72 on liver function. Serum samples were harvested 18 h after CLP and sham surgery. Liver function was determined through enzymatic analysis of glutamate oxaloacetate transaminase (GOT) (a) and glutamate pyruvate transaminase (GPT) (b). Experiments were conducted as described in Section 2. Values are mean ± standard error of the mean. Each group contained 12 animals. ∗∗p < 0.01 and N.S. versus sham.

Mentions: Plasma GOT and GPT activities were significantly augmented by 126% and 121%, respectively (∗∗p < 0.01), 18 h after CLP (Figure 1, comparison between empty and black columns). The sepsis-induced increases in GOT/GPT activities returned to the control level following rhHsp72 administration (Figure 1, comparison between empty and shaded columns), demonstrating that rhHsp72 ameliorates liver function during sepsis progression.


Role of Exogenous Hsp72 on Liver Dysfunction during Sepsis.

Tsai TN, Ho JJ, Liu MS, Lee TY, Lu MC, Liu CJ, Huang LJ, Lue SI, Yang RC - Biomed Res Int (2015)

Effects of rhHsp72 on liver function. Serum samples were harvested 18 h after CLP and sham surgery. Liver function was determined through enzymatic analysis of glutamate oxaloacetate transaminase (GOT) (a) and glutamate pyruvate transaminase (GPT) (b). Experiments were conducted as described in Section 2. Values are mean ± standard error of the mean. Each group contained 12 animals. ∗∗p < 0.01 and N.S. versus sham.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4499656&req=5

fig1: Effects of rhHsp72 on liver function. Serum samples were harvested 18 h after CLP and sham surgery. Liver function was determined through enzymatic analysis of glutamate oxaloacetate transaminase (GOT) (a) and glutamate pyruvate transaminase (GPT) (b). Experiments were conducted as described in Section 2. Values are mean ± standard error of the mean. Each group contained 12 animals. ∗∗p < 0.01 and N.S. versus sham.
Mentions: Plasma GOT and GPT activities were significantly augmented by 126% and 121%, respectively (∗∗p < 0.01), 18 h after CLP (Figure 1, comparison between empty and black columns). The sepsis-induced increases in GOT/GPT activities returned to the control level following rhHsp72 administration (Figure 1, comparison between empty and shaded columns), demonstrating that rhHsp72 ameliorates liver function during sepsis progression.

Bottom Line: Apoptosis was determined using terminal deoxynucleotidyl transferase dUTP nick end labeling staining.B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), cleaved caspase-3 and caspase-9, and cleaved poly (ADP-ribose) polymerase (PARP) protein expressions were analyzed using Western blotting.The Bcl-2/Bax ratio, cleaved caspase-3, caspase-9, and PARP protein expressions in the liver tissues were upregulated during sepsis and normalized after rhHsp72 treatment.

View Article: PubMed Central - PubMed

Affiliation: Graduate Institute of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.

ABSTRACT
This study examined the role of exogenous heat shock protein 72 (Hsp72) in reversing sepsis-induced liver dysfunction. Sepsis was induced by cecal ligation and puncture. Liver function was determined on the basis of the enzymatic activities of serum glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT). Apoptosis was determined using terminal deoxynucleotidyl transferase dUTP nick end labeling staining. B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), cleaved caspase-3 and caspase-9, and cleaved poly (ADP-ribose) polymerase (PARP) protein expressions were analyzed using Western blotting. Results showed GOT and GPT levels increased during sepsis, and levels were restored following the administration of human recombinant Hsp72 (rhHsp72). Increased liver tissue apoptosis was observed during sepsis, and normal apoptosis resumed on rhHsp72 administration. The Bcl-2/Bax ratio, cleaved caspase-3, caspase-9, and PARP protein expressions in the liver tissues were upregulated during sepsis and normalized after rhHsp72 treatment. We conclude that, during sepsis, exogenous Hsp72 restored liver dysfunction by inhibiting apoptosis via the mitochondria-initiated caspase pathway.

No MeSH data available.


Related in: MedlinePlus