anti fibrotic potential of noni n.
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ANTI FIBROTIC POTENTIAL OF NONI

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ANTI FIBROTIC POTENTIAL OF NONI

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  1. ANTI FIBROTIC POTENTIAL OF NONI

  2. Liver Fibrosis • Liver Fibrosis is Characterized by • Excessive Scarring • Excessive Production and deposition of Collagens • (elastin and laminin) • 3. Decreased Collagenolytic activity (1) • 4. Altered Extra cellular matrix ( ECM )

  3. Biochemical Marker Hydroxy Proline ( HP) Altered ECM – Major producer of fibrotic neomatrix Altered ECM – excess collagen - Triple Helix structure Stabilized by Hydroxy Proline

  4. Altered ECM Degraded by Matrix Metallo Proteinase (MMP) 2 & 3 Inhibited by Tissue Inhibitors of MMP ( TIMPS) In fibrosis Excessive Production of TIMPS TIMPS expression correlates with HP

  5. INDUCTION Liver fibrosis – results of repeated repair of chronic liver damage. Chronic Liver injury – chemicals – CCl4. Single dose – Liver Damage Repeated doses – Chronic Liver damage.

  6. Materials and Methods Animals - Male Albino Wistar rats Groups I - Normal II - CCL4 -1 ml/kg mixed with equal volume of liquid paraffin twice a week for 4 weeks (4) III - “ + 5 ml of diluted Noni extract in divided doses.

  7. Biochemical Parameters Aspartate Transaminase (AST – IU/L) Alanine Transaminase (ALT – IU/L) Alkaline Phosphatase ( ALP – IU/L) Total Bilirubin (TBL – mg/dl) Hydroxyproline (HP – mg/g of liver) Other Parameters Body Weight Liver Weight

  8. Effect of Noni on biochemical Parameter AST ( IU/L) ALT ( IU/L) ALP ( IU/L) TBL (mg/dl) HP (μg/g of liver tissue) GROUPS Groups I 159 ± 6 47 ± 2 215 ± 7 0.48 ± .01 53 ± 3 II 289 ± 11* 102 ± 5* 396 ± 8* 1.6 ± .08* 124 ± 7* III 175 ± 8*a 61 ± 4*a 235 ± 12*a 0.7 ± 0.3*a 77 ± 3*a • Significantly different from Group –I • *a Significantly different from Group - II

  9. Effect of Noni on liver and Body weight Body Weight GROUPS Liver Weight on Day 28 Day 28 Day 1 I 163 ± 4 3.4 ± 0.3 164 ± 3 165 ± 3 II 148±2* 4.5 ±0.06* 3.8 ± 0.05*a III 164 ± 2 159 ±2*a • Significantly different from Group –I • *a Significantly different from Group - II

  10. DISCUSSION • Hepatic stellate cells of Liver are associated with fibrosis • Normally – Vit A stores • Chronic injury – proliferation Excessive secretion of collagen Altered ECM HP

  11. Level of HP correlates with the extent of fibrosis • Scope for future study • CCL4  CCL3 (free radical)  Lipid peroxidation Liver damage • Antioxidant potential  confirms the antifibrotic potential

  12. CONCLUSION • AST, ALT, ALP, TBL levels confirm the hepato protective potential • HP level in group III indicate the antifibrotic potential of NONI

  13. references • Okazaki, I., Maruyama, K.,1974. Collagenase activity in experimental hepatic fibrosis. Nature 252, 49-50. • Arthur, M.J.P., 1997. Matrix degradation in liver and a role in injury and repair. Hepatalogy 26, 1069-1071. • Ohuchi, E., Imai, E., Fijii, Y., 1997. Membrane type I matrix metalloproteinases digests interstitial collagens and other extra cellular matrix macromolecules.J.Biol.Chem.272,2446-2451. • Bickel, M., Baader, E., Brocks, D.G., Engelbart, K., Gunzler, V., Schmidts, H.L., Vogel, G.H., 1991.Beneficial effects of inhibitors of propyl 4-hydroxylase in CCl4 induced fibrosis of liver in rats.J.Hepatol.13 (Suppl.3),26-33.

  14. THANKING YOU