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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 apoptosis inhibition in livers of rats with sepsis. Experiments were conducted as described in Section 2. Panel (a) plots the representative histograms of TUNEL and hematoxylin staining (sham: (A) and (D); CLP: (B) and (E); CLP+rhHsp72: (C) and (F)). Panel (b) depicts the quantitative analysis of TUNEL-/hematoxylin-positive cells. Values (means ± SE) presented in Panel (b) were obtained by dividing the number of TUNEL-positive cells by the total number of nucleoli. Each group contained 12 animals. ∗∗p < 0.01 and N.S. versus sham.
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fig2: Effects of rhHsp72 on apoptosis inhibition in livers of rats with sepsis. Experiments were conducted as described in Section 2. Panel (a) plots the representative histograms of TUNEL and hematoxylin staining (sham: (A) and (D); CLP: (B) and (E); CLP+rhHsp72: (C) and (F)). Panel (b) depicts the quantitative analysis of TUNEL-/hematoxylin-positive cells. Values (means ± SE) presented in Panel (b) were obtained by dividing the number of TUNEL-positive cells by the total number of nucleoli. Each group contained 12 animals. ∗∗p < 0.01 and N.S. versus sham.

Mentions: The extent of sepsis-induced cell apoptosis was detected using TUNEL staining (Figure 2(a)). As shown in Figure 2(b), significant increases in the number of TUNEL-positive cells (21.7%) were observed in the CLP group. Sepsis increased the number of TUNEL-positive cells by 6.6 times (+665.7%) (Figure 2(b), comparison between black and empty columns), whereas the sepsis-induced augmentation in TUNEL-positive cells returned to the control level after rhHsp72 administration (Figure 2(b), comparison between empty and shaded columns; N.S.). These results indicate that exogenous Hsp72 protects liver cells from cell death 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 apoptosis inhibition in livers of rats with sepsis. Experiments were conducted as described in Section 2. Panel (a) plots the representative histograms of TUNEL and hematoxylin staining (sham: (A) and (D); CLP: (B) and (E); CLP+rhHsp72: (C) and (F)). Panel (b) depicts the quantitative analysis of TUNEL-/hematoxylin-positive cells. Values (means ± SE) presented in Panel (b) were obtained by dividing the number of TUNEL-positive cells by the total number of nucleoli. Each group contained 12 animals. ∗∗p < 0.01 and N.S. versus sham.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4499656&req=5

fig2: Effects of rhHsp72 on apoptosis inhibition in livers of rats with sepsis. Experiments were conducted as described in Section 2. Panel (a) plots the representative histograms of TUNEL and hematoxylin staining (sham: (A) and (D); CLP: (B) and (E); CLP+rhHsp72: (C) and (F)). Panel (b) depicts the quantitative analysis of TUNEL-/hematoxylin-positive cells. Values (means ± SE) presented in Panel (b) were obtained by dividing the number of TUNEL-positive cells by the total number of nucleoli. Each group contained 12 animals. ∗∗p < 0.01 and N.S. versus sham.
Mentions: The extent of sepsis-induced cell apoptosis was detected using TUNEL staining (Figure 2(a)). As shown in Figure 2(b), significant increases in the number of TUNEL-positive cells (21.7%) were observed in the CLP group. Sepsis increased the number of TUNEL-positive cells by 6.6 times (+665.7%) (Figure 2(b), comparison between black and empty columns), whereas the sepsis-induced augmentation in TUNEL-positive cells returned to the control level after rhHsp72 administration (Figure 2(b), comparison between empty and shaded columns; N.S.). These results indicate that exogenous Hsp72 protects liver cells from cell death 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