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Renoprotection by alpha-Mangostin is related to the attenuation in renal oxidative/nitrosative stress induced by cisplatin nephrotoxicity. Pérez-Rojas JM, Cruz C, García-López P, Sánchez-González DJ, Martínez-Martínez C Ceballos G, sp!nosa M, Melén"ez-#aj$la J, Pe"raza-Cha%err! J& Source 'aculta" "e (uí)!ca, Departa)ento "e *!olo$ía, +n!%ers!"a" ac!onal utóno)a "e Mé.!co, "!/!c!o ', Me.!co C!t0, Me.!co& Abstract C!splat!n 1CDDP2 !s a che)otherapeut!c a$ent that pro"uces nephroto.!c!t0 assoc! o.!"at!%e4n!trosat!%e stress& alpha-Man$ost!n 1alpha-M2 !s a .anthone e.tracte" )an$osteen 3!th ant!o.!"ant an" ant!-!n/la))ator0 propert!es& 5he purpose o/ th! to e%aluate the renoprotect!%e e//ect o/ alpha-M on the CDDP-!n"uce" nephroto.!c M 3as a")!n!stere" 167&8 )$49$4"a0, !&$&2 /or 6: "a0s 1; "a0s be/ore an" < "a0s !nject!on2& =n "a0 ;, rats 3ere treate" 3!th a s!n$le !nject!on o/ CDDP 1;&8 )$4 "a0s a/ter the rats 3ere 9!lle"& alpha-M attenuate" renal "0s/unct!on, structura o.!"at!%e4n!trosat!%e stress, "ecrease !n catalase e.press!on an" !ncrease !n )R tu)our necros!s /actor alpha an" trans/or)!n$ $ro3th /actor beta& @n conclus!on renoprotect!%e e//ect o/ alpha-M on CDDP-!n"uce" nephroto.!c!t0 3as assoc!ate" 3 attenuat!on !n o.!"at!%e4n!trosat!%e stress an" !n/la))ator0 an" /!brot!c )ar9er preser%at!on o/ catalase act!%!t0& http://www.ncbi.nlm.nih.gov/pubmed/19863372

Xanthone Kidney

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Xanthone Kidney

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Renoprotection by alpha-Mangostin is related to the attenuation in renal oxidative/nitrosative stress induced by cisplatin nephrotoxicity.Prez-Rojas JM, Cruz C, Garca-Lpez P, Snchez-Gonzlez DJ, Martnez-Martnez CM, Ceballos G, Espinosa M, Melndez-Zajgla J, Pedraza-Chaverri J.SourceFacultad de Qumica, Departamento de Biologa, Universidad Nacional Autnoma de Mxico, Edificio F, Mexico City, Mexico.AbstractCisplatin (CDDP) is a chemotherapeutic agent that produces nephrotoxicity associated with oxidative/nitrosative stress. alpha-Mangostin (alpha-M) is a xanthone extracted from mangosteen with antioxidant and anti-inflammatory properties. The purpose of this study was to evaluate the renoprotective effect of alpha-M on the CDDP-induced nephrotoxicity. alpha-M was administered (12.5 mg/kg/day, i.g.) for 10 days (7 days before and 3 days after CDDP injection). On day 7, rats were treated with a single injection of CDDP (7.5 mg/Kg, i.p.); 3 days after the rats were killed. alpha-M attenuated renal dysfunction, structural damage, oxidative/nitrosative stress, decrease in catalase expression and increase in mRNA levels of tumour necrosis factor alpha and transforming growth factor beta. In conclusion the renoprotective effect of alpha-M on CDDP-induced nephrotoxicity was associated with the attenuation in oxidative/nitrosative stress and inflammatory and fibrotic markers and preservation of catalase activity.http://www.ncbi.nlm.nih.gov/pubmed/19863372

The alpha-mangostin prevention on cisplatin-induced apoptotic death in LLC-PK1 cells is associated to an inhibition of ROS production and p53 induction.Snchez-Prez Y, Morales-Brcenas R, Garca-Cuellar CM, Lpez-Marure R, Calderon-Oliver M, Pedraza-Chaverri J, Chirino YI.SourceSubdireccin de Investigacin Bsica, Instituto Nacional de Cancerologa, San Fernando No. 22, Tlalpan, 14080 Mexico, DF, Mexico.AbstractCisplatin (CDDP) is a widely useful chemotherapeutic agent for the treatment of tumors including lung, ovary and testis. Acute renal injury, however, is the main side effect observed after CDDP treatment. This side effect is related to the apoptotic death in proximal tubular cells in the kidney and p53 protein has a central role in this process. On the other hand, alpha-mangostin (alpha-M), a xanthone derived from the pericarp of mangosteen, exerts a renoprotective effect against cisplatin-induced renal damage in rats. The aim of this study was to evaluate whether alpha-M protects proximal tubule renal epithelial cells (LLC-PK1) from CDDP-induced apoptotic death. Cells were co-incubated with 5 microM alpha-M and 100 microM CDDP for 24h. It was found that alpha-M attenuated the following alterations: the apoptotic cell death, the increase in reactive oxygen species (ROS), the glutathione depletion and the increase in p53 expression induced by CDDP. In conclusion, the preventive effect of alpha-M on CDDP-induced apoptotic death is associated to the inhibition of p53 expression and ROS generation.http://www.ncbi.nlm.nih.gov/pubmed/20603111