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Role of sulphated polysaccharides from Sargassum Wightii in Cyclosporine A-induced oxidative liver injury in rats.

Josephine A, Nithya K, Amudha G, Veena CK, Preetha SP, Varalakshmi P - BMC Pharmacol. (2008)

Bottom Line: This in turn led to enhanced levels of lipid peroxidation, 8-hydroxy-2-deoxy guanosine and protein carbonyls, along with a decrease in ATPase activities and alterations in lipid profile.Histopathological changes also strongly support the above aberrations.However, concomitant treatment with sulphated polysaccharides restored the above deformities to near control and prevented the morphological alterations significantly.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Medical Biochemistry, Dr, ALM, Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai - 600 113, India. ajose_joy@yahoo.co.in

ABSTRACT

Background: Seaweeds or marine algae have long been made up a key part of the Asian diet, and as an antioxidant, sulphated polysaccharides have piqued the interest of many researchers as one of the ocean's greatest treasures. The present investigation suggests the therapeutic potential of sulphated polysaccharides from marine brown algae "Sargassum wightii" in Cyclosporine A (CsA)- induced liver injury. CsA is a potent immunosuppressive agent used in the field of organ transplantations and various autoimmune disorders. However, hepatotoxicity due to CsA remains to be one of the major clinical challenges.

Methods: The effect of sulphated polysaccharides on CsA-induced hepatotoxicity was studied in adult male albino rats of Wistar strain, and the animals were randomized into four groups with six rats in each. Group I served as vehicle control. Group II rats were given CsA at a dosage of 25 mg/kg body weight, orally for 21 days. Group III rats were given sulphated polysaccharides at a dosage of 5 mg/kg body weight, subcutaneously for 21 days. Group IV rats were given sulphated polysaccharides simultaneously along with CsA, as mentioned in Group II for 21 days.

Results: CsA provoked hepatotoxicity was evident from the decreased activities of hepatic marker enzymes. A significant rise in the level of oxidants, along with a striking decline in both the enzymic and non-enzymic antioxidants, marks the severity of oxidative stress in CsA-induced rats. This in turn led to enhanced levels of lipid peroxidation, 8-hydroxy-2-deoxy guanosine and protein carbonyls, along with a decrease in ATPase activities and alterations in lipid profile. Histopathological changes also strongly support the above aberrations. However, concomitant treatment with sulphated polysaccharides restored the above deformities to near control and prevented the morphological alterations significantly.

Conclusion: Thus, the present study highlights that sulphated polysaccharides can act therapeutically against CsA-induced hepatotoxicity.

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Histopathological findings in the liver tissue of CsA-induced and treated groups. Control and drug control groups show normal liver architecture (Figure 3a and 3c). Liver sections treated with CsA produces marked changes like inflammation around portal triad (Triaditis) with patchy microvesicular fatty degeneration (Figure 3b). Sulphated polysaccharides treated rats (Figure 3d) show considerable reduction in the pathological changes compared to CsA-induced animals.
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Figure 3: Histopathological findings in the liver tissue of CsA-induced and treated groups. Control and drug control groups show normal liver architecture (Figure 3a and 3c). Liver sections treated with CsA produces marked changes like inflammation around portal triad (Triaditis) with patchy microvesicular fatty degeneration (Figure 3b). Sulphated polysaccharides treated rats (Figure 3d) show considerable reduction in the pathological changes compared to CsA-induced animals.

Mentions: Histopathological findings in liver sections (H & E, 100×) from the four experimental groups are highlighted in Figure 3. Control and drug control groups showed normal liver architecture (Figures 3a and 3c). Liver sections treated with CsA produced marked changes like inflammation around portal triad (Triaditis) with patchy microvesicular fatty degeneration (Figure 3b). Sulphated polysaccharides treated Group IV rats (Figure 3d) showed considerable reduction in the pathological changes as seen in CsA induced animals and exhibited almost normal architecture as that of controls.


Role of sulphated polysaccharides from Sargassum Wightii in Cyclosporine A-induced oxidative liver injury in rats.

Josephine A, Nithya K, Amudha G, Veena CK, Preetha SP, Varalakshmi P - BMC Pharmacol. (2008)

Histopathological findings in the liver tissue of CsA-induced and treated groups. Control and drug control groups show normal liver architecture (Figure 3a and 3c). Liver sections treated with CsA produces marked changes like inflammation around portal triad (Triaditis) with patchy microvesicular fatty degeneration (Figure 3b). Sulphated polysaccharides treated rats (Figure 3d) show considerable reduction in the pathological changes compared to CsA-induced animals.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2291455&req=5

Figure 3: Histopathological findings in the liver tissue of CsA-induced and treated groups. Control and drug control groups show normal liver architecture (Figure 3a and 3c). Liver sections treated with CsA produces marked changes like inflammation around portal triad (Triaditis) with patchy microvesicular fatty degeneration (Figure 3b). Sulphated polysaccharides treated rats (Figure 3d) show considerable reduction in the pathological changes compared to CsA-induced animals.
Mentions: Histopathological findings in liver sections (H & E, 100×) from the four experimental groups are highlighted in Figure 3. Control and drug control groups showed normal liver architecture (Figures 3a and 3c). Liver sections treated with CsA produced marked changes like inflammation around portal triad (Triaditis) with patchy microvesicular fatty degeneration (Figure 3b). Sulphated polysaccharides treated Group IV rats (Figure 3d) showed considerable reduction in the pathological changes as seen in CsA induced animals and exhibited almost normal architecture as that of controls.

Bottom Line: This in turn led to enhanced levels of lipid peroxidation, 8-hydroxy-2-deoxy guanosine and protein carbonyls, along with a decrease in ATPase activities and alterations in lipid profile.Histopathological changes also strongly support the above aberrations.However, concomitant treatment with sulphated polysaccharides restored the above deformities to near control and prevented the morphological alterations significantly.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Medical Biochemistry, Dr, ALM, Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai - 600 113, India. ajose_joy@yahoo.co.in

ABSTRACT

Background: Seaweeds or marine algae have long been made up a key part of the Asian diet, and as an antioxidant, sulphated polysaccharides have piqued the interest of many researchers as one of the ocean's greatest treasures. The present investigation suggests the therapeutic potential of sulphated polysaccharides from marine brown algae "Sargassum wightii" in Cyclosporine A (CsA)- induced liver injury. CsA is a potent immunosuppressive agent used in the field of organ transplantations and various autoimmune disorders. However, hepatotoxicity due to CsA remains to be one of the major clinical challenges.

Methods: The effect of sulphated polysaccharides on CsA-induced hepatotoxicity was studied in adult male albino rats of Wistar strain, and the animals were randomized into four groups with six rats in each. Group I served as vehicle control. Group II rats were given CsA at a dosage of 25 mg/kg body weight, orally for 21 days. Group III rats were given sulphated polysaccharides at a dosage of 5 mg/kg body weight, subcutaneously for 21 days. Group IV rats were given sulphated polysaccharides simultaneously along with CsA, as mentioned in Group II for 21 days.

Results: CsA provoked hepatotoxicity was evident from the decreased activities of hepatic marker enzymes. A significant rise in the level of oxidants, along with a striking decline in both the enzymic and non-enzymic antioxidants, marks the severity of oxidative stress in CsA-induced rats. This in turn led to enhanced levels of lipid peroxidation, 8-hydroxy-2-deoxy guanosine and protein carbonyls, along with a decrease in ATPase activities and alterations in lipid profile. Histopathological changes also strongly support the above aberrations. However, concomitant treatment with sulphated polysaccharides restored the above deformities to near control and prevented the morphological alterations significantly.

Conclusion: Thus, the present study highlights that sulphated polysaccharides can act therapeutically against CsA-induced hepatotoxicity.

Show MeSH
Related in: MedlinePlus