Volume 18, Issue 2, Pages (April 2011)

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Volume 18, Issue 2, Pages 125-135 (April 2011) Antioxidant and antiapoptotic effects of green tea polyphenols against azathioprine- induced liver injury in rats  Hesham A. El-Beshbishy, Ola M. Tork, Mohamed F. El-Bab, Mohamed A. Autifi  Pathophysiology  Volume 18, Issue 2, Pages 125-135 (April 2011) DOI: 10.1016/j.pathophys.2010.08.002 Copyright © 2010 Elsevier Ireland Ltd Terms and Conditions

Fig. 1 Serum (A) sALT, (B) sAST, (C) sALP and (D) total proteins levels of normal control, GTP100, GTP300, AZA-intoxicated, AZA-GTP100 and AZA-GTP300 rats. Data represent the means±SEM (n=8). *Significant change difference compared to AZA-intoxicated rats, p<0.001. †Significant difference compared to normal control rats, p<0.001. Pathophysiology 2011 18, 125-135DOI: (10.1016/j.pathophys.2010.08.002) Copyright © 2010 Elsevier Ireland Ltd Terms and Conditions

Fig. 2 Liver (A) MDA, (B) total antioxidant activity TAA, and (C) protein carbonyl content levels of normal control, GTP100, GTP300, AZA-intoxicated, AZA-GTP100 and AZA-GTP300 rats. Data represent the means±SEM (n=8). *Significant change difference compared to AZA-intoxicated rats, P<0.001. †Significant difference compared to normal control rats, p<0.001. Pathophysiology 2011 18, 125-135DOI: (10.1016/j.pathophys.2010.08.002) Copyright © 2010 Elsevier Ireland Ltd Terms and Conditions

Fig. 3 Liver (A) GPx, (B) CAT, (C) GSH, (D) GSSG and GSH/GSSG levels of normal control, GTP100, GTP300, AZA-intoxicated, AZA-GTP100 and AZA-GTP300 rats. Data represent the means±SEM (n=8). *Significant change difference compared to AZA-intoxicated rats, p<0.001. †Significant difference compared to normal control rats, p<0.001. Pathophysiology 2011 18, 125-135DOI: (10.1016/j.pathophys.2010.08.002) Copyright © 2010 Elsevier Ireland Ltd Terms and Conditions

Fig. 4 Liver (A) TNF-α and (B) caspase-3-activity of normal control, GTP100, GTP300, AZA-intoxicated, AZA-GTP100 and AZA-GTP300 rats. Data represent the means±SEM (n=8). *Significant change difference compared to AZA-intoxicated rats, p<0.001. †Significant difference compared to normal control rats, p<0.001. Pathophysiology 2011 18, 125-135DOI: (10.1016/j.pathophys.2010.08.002) Copyright © 2010 Elsevier Ireland Ltd Terms and Conditions

Fig. 5 Linear regression analysis showed the correlation of sALT, sAST, sALP or liver GPx (A), liver MDA, TAA, protein carbonyl content or caspase-3 levels (B), liver CAT, GSH or GSSG (C) of AZA-GTP100 rats, and sALT, sAST, sALP or liver GPx (D), liver MDA, TAA, protein carbonyl content or caspase-3 levels (E), liver CAT, GSH or GSSG (F) of AZA-GTP300 rats, on hepatic TNF-α after oral administration of either GTP100 or GTP300 to AZA-intoxicated rats. Pathophysiology 2011 18, 125-135DOI: (10.1016/j.pathophys.2010.08.002) Copyright © 2010 Elsevier Ireland Ltd Terms and Conditions

Fig. 6 Microscopic view of liver section obtained from normal control, GTP100, GTP300, AZA, AZA-GTP100 and AZA-GTP300 rats stained with hematoxylin and eosin 200×. Photomicrograph of liver section of: (A) normal control rat showing normal hepatic architecture. Hepatocytes (H) radiating from central veins (CV). The blood sinusoids (S) open into central veins. (B) Normal GTP100 rat showing normal structure of hepatic lobules and hepatocytes. (C) Normal GTP300 rat showing the hepatocytes appearing normal and radiating from the central vein (CV). The blood sinusoids (S) are normal and alternating with the hepatic lobules. (D) AZA rat showing area of hepatocytes degeneration (D) and dilated blood sinusoids (S). Central veins (CV) appeared widely separated. Area of hemorrhage and inflammatory cell infiltration (HG) around blood sinusoids are seen. (E) AZA-GTP100 rat showing some areas of swelling and degeneration of hepatocytes. The rest of the hepatocytes showing normal appearance. Blood sinusoids are widely separated and showing area of congestion and inflammatory cell infiltration (S). (F) AZA-GTP300 rat showing normal appearance of hepatocytes with preservation of normal hepatic architecture. Pathophysiology 2011 18, 125-135DOI: (10.1016/j.pathophys.2010.08.002) Copyright © 2010 Elsevier Ireland Ltd Terms and Conditions