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La retinopatia diabetica è una patologia complessa sempre alla ricerca di nuovi orizzonti terapeutici.
La letteratura recente dimostra che il diabete determina un eccesso di anione superossido da parte della catena di trasporto mitocondriale. Da tale evento sembrano scaturire i danni propri della sindrome diabetica.
Il danno che si manifesta a carico del tessuto retinico è duplice:
danno neurosensoriale: è presente in fase precoce ed è evidenziabile anche in assenza di retinopatia diabetica
danno vascolare: è più tardivo, con possibile neoangiogenesi.
E' necessario intervenire già nella fase iniziale della malattia con rimedi adeguati a prevenire l'aggravamento del quadro clinico o, per lo meno, a stabilizzarne il suo decorso. L'intervento terapeutico si avvale di un accurato controllo del diabete e della somministrazione di preparati in grado di esercitare un positivo influsso sulla componente vascolare e metabolica dei tessuti oculari, in particolare della retina.

 
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Info in Vista 2006 N.1 RETINOPARIA DIABETICA

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Bibliografia

1. Kowluru RA. Diabetic retinopathy: mitochondrial dysfunction and retinal capillary cell death. Antioxid Redox Signal. 2005 Nov-Dec;7(11-12):1581-87. Review.

2. Vincent AM, Olzmann JA, Brownlee M, Sivitz WI, Russell JW. Uncoupling proteins prevent glucose-induced neuronal oxidative stress and programmed cell death. Diabetes. 2004 Mar;53(3):726-34.

3. Huang TJ, Price SA, Chilton L, Calcutt NA, Tomlinson DR, Verkhratsky A, Fernyhough P. Insuli prevents depolarization of the mitochondrial inner membrane in sensory neurons of type 1 diabetic rats in the presence of sustained hyperglycemia. Diabetes. 2003 Aug;52(8):2129-36.

4. Chung SS, Ho EC, Lam KS, Chung SK. Contribution of polyol pathway to diabetes-induced oxidative stress. J Am Soc Nephrol. 2003 Aug;14(8 Suppl 3):S233-6. Review

5. Russell JW, Golovoy D, Vincent AM, Mahendru P, Olzmann JA, Mentzer A, Feldman EL. High glucose-induced oxidative stress and mitochondrial dysfunction in neurons. FASEB J. 2002 Nov;16(13):1738-48.

6. Nishikawa T, Edelstein D, Du XL, Yamagishi S, Matsumura T, Kaneda Y, Yorek MA, Beebe D, Oates PJ, Hammes HP, Giardino I, Brownlee M. Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature. 2000 Apr 13;404(6779):787-90.

7. Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature. 2001 Dec 13;414(6865):813-20.

8. Du X, Matsumura T, Edelstein D, Rossetti L, Zsengeller Z, Szabo C, Brownlee M. Inhibition of GAPDH activity by poly(ADP-ribose) polymerase activates three major pathways of hyperglycemic damage in endothelial cells. J Clin Invest. 2003 Oct;112(7):1049-57.

9. Obrosova IG, Li F, Abatan OI, Forsell MA, Komjati K, Pacher P, Szabo C, Stevens MJ. Role of poly(ADP-ribose) polymerase activation in diabetic neuropathy. Diabetes. 2004 Mar;53(3):711-20.

10. Spitaler MM, Graier WF. Vascular targets of redox signalling in diabetes mellitus. Diabetologia. 2002 Apr;45(4):476-94. Review.

11. Ceriello A. New insights on oxidative stress and diabetic complications may lead to a "causal" antioxidant therapy. Diabetes Care. 2003 May;26(5):1589-96. Review.

12. Han Y, Bearse MA Jr, Schneck ME, Barez S, Jacobsen CH, Adams AJ. Related Articles, Links Multifocal electroretinogram delays predict sites of subsequent diabetic retinopathy. Invest Ophthalmol Vis Sci. 2004 Mar;45(3):948-54.

13. Bearse MA Jr, Han Y, Schneck ME, Adams AJ. Related Articles, Links Retinal function in normal and diabetic eyes mapped with the slow flash multifocal electroretinogram. Invest Ophthalmol Vis Sci. 2004 Jan;45(1):296-304.

14. Lund-Andersen C, Frost-Larsen K, Starup K. Acta Ophthalmol (Copenh). 1987 Aug;65(4):481-6 Natural history of diabetic retinopathy in insulin-dependent juvenile diabetics. A longitudinal study.

15. Chidlow G, Schmidt KG, Wood JP, Melena J, Osborne NN. Alpha-lipoic acid protects the retina against ischemia-reperfusion. Neuropharmacology. 2002 Nov;43(6):1015-25.

16. Low PA, Nickander KK, Tritschler HJ. The roles of oxidative stress and antioxidant treatment in experimental diabetic neuropathy. Diabetes. 1997 Sep;46 Suppl 2:S38-42.

17. van Dam PS. Oxidative stress and diabetic neuropathy: pathophysiological mechanisms and treatment perspectives. Diabetes Metab Res Rev. 2002 May-Jun;18(3):176-84. Review.

18. Baydas G, Donder E, Kiliboz M, Sonkaya E, Tuzcu M, Yasar A, Nedzvetskii VS. Neuroprotection by alpha-lipoic acid in streptozotocin-induced diabetes. Biochemistry (Mosc). 2004 Sep;69(9):1001-5.

19. Stevens MJ, Obrosova I, Cao X, Van Huysen C, Greene DA. Effects of DL-alpha-lipoic acid on peripheral nerve conduction, blood flow, energy metabolism, and oxidative stress in experimental diabetic neuropathy. Diabetes. 2000 Jun;49(6):1006-15.

20. Packer L, Kraemer K, Rimbach G. Molecular aspects of lipoic acid in the prevention of diabetes complications. Nutrition. 2001 Oct;17(10):888-95. Review.

21. Nickander KK, McPhee BR, Low PA, Tritschler H. Alpha-lipoic acid: antioxidant potency against lipid peroxidation of neural tissues in vitro and implications for diabetic neuropathy. Free Radic Biol Med. 1996;21(5):631-9.

22. Baydas G, Donder E, Kiliboz M, Sonkaya E, Tuzcu M, Yasar A, Nedzvetskii VS Neuroprotection by alpha-lipoic acid in streptozotocin-induced diabetes. Biochemistry (Mosc). 2004 Sep;69(9):1001-5. 26)

23. Morris TW, Reed KE, Cronan JE Jr. Lipoic acid metabolism in Escherichia coli: the lplA and lipB genes define redundant pathways for ligation of lipoyl groups to apoprotein. J Bacteriol. 1995 Jan;177(1):1-10.

24. Kolobova E, Tuganova A, Boulatnikov I, Popov KM. Regulation of pyruvate dehydrogenase activity through phosphorylation at multiple sites. Biochem J. 2001 Aug 15;358(Pt 1):69-77.

25. Packer L, Witt EH, Tritschler HJ. alpha-Lipoic acid as a biological antioxidant. Free Radic Biol Med. 1995 Aug;19(2):227-50. Review.

26. Biewenga GP, Haenen GR, Bast A. The pharmacology of the antioxidant lipoic acid. Gen Pharmacol. 1997 Sep;29(3):315-31. Review.

27. Kowluru RA, Odenbach S. Effect of long-term administration of alpha-lipoic acid on retinal capillary cell death and the development of retinopathy in diabetic rats. Diabetes. 2004 Dec;53(12):3233-8.

28. Campbell N A Biologia Zanichelli

29. Davidson GE et all The metabolic conseguences of vitamin B12 / methionine deficienty in rats. Biochim biophiys acta 1975 jun 12;392(2): 207 - 215

30. Murata M, Kador PF, Sato S. Vascular endothelial growth factor (EGF) enhances the expression of receptors and activates mitogen-activated protein (MAP) kinase of dog retinal capillary endothelial cells. J Ocul Pharmacol Ther. 2000 Aug;16(4):383-91.

31. Akiyama T, Ishida J, Nakagawa S, Ogawara H, Watanabe S, Itoh N, Shibuya M, Fukami Y. Genistein, a specific inhibitor of tyrosine-specific protein kinases. J Biol Chem. 1987 Apr 25;262(12):5592-5.

32. Hayashi A, Weinberger AW, Kim HC, de Juan E Jr. Genistein, a protein tyrosine kinase inhibitor, ameliorates retinal degeneration after ischemia- reperfusion injury in rat. Invest Ophthalmol Vis Sci. 1997 May;38(6):1193-202.

33. Chung MJ, Kang AY, Lee KM, Oh E, Jun HJ, Kim SY, Auh JH, Moon TW, Lee SJ, Park KH. Water-soluble genistin glycoside isoflavones up-regulate antioxidant metallothionein expression and scavenge free radicals. J Agric Food Chem. 2006 May 31;54(11):3819-26.

34. Nakajima M, Cooney MJ, Tu AH, Chang KY, Cao J, Ando A, An GJ, Melia M, de Juan E Jr. Normalization of retinal vascular permeability in experimental diabetes with genistein. Invest Ophthalmol Vis Sci. 2001 Aug;42(9):2110-4.

35. Buchler P, Reber HA, Buchler MW, Friess H, Lavey RS, Hines OJ Antiangiogenic activity of genistein in pancreatic carcinoma cells is mediated by the inhibition of hypoxia-inducible factor-1 and the down-regulation of VEGF gene expression. Cancer. 2004 Jan 1;100(1):201-10.

36. Wang B, Li H, Yan H, Xiao JG. Genistein inhibited hypoxia-inducible factor-1alpha expression induced by hypoxia and cobalt chloride in human retinal pigment epithelium cells. Methods Find Exp Clin Pharmacol. 2005 Apr;27(3):179-84.

37. Wang B, Zou Y, Li H, Yan H, Pan JS, Yuan ZL. Genistein inhibited retinal neovascularization and expression of vascular endothelial growth factor and hypoxia inducible factor 1alpha in a mouse model of oxygen-induced retinopathy. J Ocul Pharmacol Ther. 2005 Apr;21(2):107-13.

38. Constantinescu A, Han D, Packer L. Vitamin E recycling in human erythrocyte membranes. J Biol Chem. 1993 May 25;268(15):10906-13.

39. Kagan VE, Serbinova EA, Forte T, Scita G, Packer L. Related Articles, Links Recycling of vitamin E in human low density lipoproteins. J Lipid Res. 1992 Mar;33(3):385-97.

40. Stoyanovsky DA, Goldman R, Darrow RM, Organisciak DT, Kagan VE. Endogenous ascorbate regenerates vitamin E in the retina directly and in combination with exogenous dihydrolipoic acid. Curr Eye Res. 1995 Mar;14(3):181-9

41. Xu DP, Wells WW. alpha-Lipoic acid dependent regeneration of ascorbic acid from dehydroascorbic acid in rat liver mitochondria. J Bioenerg Biomembr. 1996 Feb;28(1):77-85.

 
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tioretin_compresse
Composizione
INFORMAZIONI NUTRIZIONALI per 1 cpr da g 0,92 %RDA
Acido Lipoico 400 mg  
Genisteina 80 mg  
Vitamina PP 8 mg 50 %
Vitamina E 6 mg 50 %
Vitamina B6 1,4 mg 100%
Vitamina B2 1,4 mg 100%
Vitamina B1 1,1 mg 100%
Vitamina C 40 mg 50%
Vitamina B12 2,5 mcg 100%
 
Descrizione

TIORETIN® è un preparato a base Vitamine (B1, B2, B6, B12, C, E, PP), con Acido Lipoico e Genisteina.
Il complesso vitaminico B consente una azione trofica in sinergia con quella esercitata da altri antiossidanti come la Vitamina C e la Vitamina E, che ne ottimizzano l’effetto antiossidante.

La particolare tecnologia utilizzata nella produzione di TIORETIN® permette di ottenere una cessione delle sostanze attive in modo diversificato. Una parte a cessione rapida (fast) viene rapidamente messa a disposizione mentre il resto del contenuto della compressa si libera lentamente (slow) attraverso un rilascio controllato nel tempo. Questa tecnologia consente una più lunga durata dell’effetto del TIORETIN®.

 
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Uso del prodotto

CAMPO D’IMPIEGO
TIORETIN® è indicato in caso di aumentato fabbisogno o di diminuito apporto con la dieta dei nutrienti che lo compongono. Contribuisce :
• al normale funzionamento del sistema nervoso (Vit. PP, Vit. B1, Vit. B2, Vit. B12);
• alla normale formazione del collagene e per la normale funzione
  dei vasi sanguigni (Vit. C);
• alla protezione delle cellule dallo stress ossidativo (Vit. C, Vit. E, Vit. B2);
• alla rigenerazione della forma ridotta della Vitamina E (Vit. C);
• al normale metabolismo delle proteine e del glicogeno (Vit. B6);
• alla normale funzione dei globuli rossi (Vit. B6, Vit. B2, Vit. B12);
• al mantenimento della capacità visiva normale (Vit. B2).

DOSE GIORNALIERA E MODALITÀ D'USO
1 compressa al giorno.

CONFEZIONE
Scatola: 2 blister da 15 compresse

 

 
 
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