Nouzari, Zohre

Simorgh Research Repository

*S..Lj1 o,rS-:,ll.l#li #y* ai,nJ .u?,rl .r-l'.,r.-'t< tt3. *l: r!!:;13"cGZLZA, )"r*lCl csl.sr5 csl^r,j 64p3uK3,,,S ,9la-*ar+",r1* tstl .,&,JIcEL^ csrl* q )l,1t .rl,r,f ,,.1 t (c-2548A) i+UJ ;j j (223A>G) J*:+l r (A445CYt*  *= Jl,i.a J ;3rJfu,13;1cEli,f o;,-a;:L',.3jt:S cs.t*l L;+")ti 3:S.r 6[!1 ;t*j,al; "rti,*,l6J.fj !,r+- ;iSo - cs*J.,.o:i J."o..,-a ;rjS.l :;3t i* ,rl't,,rl\ Y1 o- 1 Yt1 Lrl-.,,--: Jt*,,!/kerman University Of Medical SciencesFacualy of MedicineIn Partial Fulfillment of the Requirements for the Degree(MSC)Title:Association of Polymorphisms of Aperin, Leptin and Leptin GenesReceptors with the susceptibility to coronary Artery Disease andIlypertensionByZohreh NozariSupervisor:Dr. Asadi KaramAdvisor:1- Dr. Nazari2- Dr. MasoumiYear:2018.*rG oa$x)L;i p lJ'rr aJ ,.:9j Lj. ,! t" J/- y.l" , a,K,u:;, !.! et-,,) ._,{1 or;rf :i-ilrat g co*iL1.: Q:.il ;.:2f o'G; $L )l 9 )9'- ,:. ,Jf t" c-9--:1 L-, ,S;*,1 39-r9o.-x! .rrlr ,-,-",a $y.ii l,_,s.G2l24, )..:rj.lcitbr*i,ys .SL*.;i ;l e**tr *1,;k? s,ty .dL.;-l,-i"ro .:;1.:;ii r{ cStrlr"&i,.s* *)t#*lr;I , VL up .,ffi a1 yi." ._,1.,1.*.,': (C-2548A) *4 Ai e Q23A>G) OJ e (Aaa5C.r.lUysf ,iil" .,sl,Sr-.!l .51-r,-15 s Gt* -*.lr.r,,t* A Jzd;,"Jyr t? ,A256 tloi& )) :to,.,lil.,CA 9 Yt 'rlo.,S t ld 95 ,(FI'A-)CA .rr+ Y! .,f 1L;-i a, V; $p_f . 1: SNP ,,\; .s.; allt rrlgo--r F-A-) CA e VL ..rl' ,,b C y:r. * )d 70 , (l I-A ) YL .rf .,S ..,1{ CA a, )t; ij 6l ,(f{ A-)df{#ij.S e$l.(;3-lr; =y.t,s"9t { .eil DNA el,pi;l ..f ,\f o",y. rr9. roli ,sf uly.t?)n qe ,-* o;L<*+ .-lr--^-i ,-,1::"f s;y11 .r-r-; ;**- PCR-RFLP ,"9;11 orl;':;l li SNP ,,\a:.brrji 1r.g;1.:,r-;* C^-4 "c^r)S ;ry. 19'JS*tr;1 V;,t ,J.i I Y!,_rl',,h 69) )1 \^\*y; Ji;**.Jr6.r^; ".!,5 p; ,t . l.Arol;o925L+u--l,Llr['lA I'{-.A'o9fr.:rs11544314.r;ny;GU*c-r*tcs.,Kij o9l-0,:Lrcit-,-lrA.-[-]i .rl:11 .5115-;1 tyL *.rslliTlUl p**6rr J, rrr r.:.(p:./. . ,I::.1.. !^r,.,p a,)r; o-r,-:J*,,, ,rs11544374 p-'';-)t" J o;15 r": ..ri"-f., lLl eU .(P:./.Y ) c-l;eli; G ,ili ! a--U",,-tl,c.r:.57ir .r:* utf a.1 CiG \4i} s) ..+ jLr &U;;lr*, (AA VS ACi+66; ;;:S;t4 ;a;(OR: 0.a0; 95% Cl: H-A- ,ul; 1) sgor I (OIi: 0.12:95% CI : 0.02*0,61 I p : 0.01) CAD.:;1.: ,_;:tsb.. ll 0.1 7-0.98: p : 0.0-l r;9rK-"lt;l r Y! ,;f ,L;s a- yli .<--) ! O*irl "s;*5 ;j rs I I 544374 ,.-*p.,r"J :6r,,!a>,,;;;9s ;u'xs ,.ribrir.. J*l' ."(,- ulr" + ;-l ;5* rs I I 37101 ,"+)rLsr A JLli ai e tf i,--l o,,o;a.tyi oy,>a CAD t ol,.o-r ', -*.-# .SLn.j sL*.:S>,tf ,gep ;elS,-\9.y{ N! "rro ,,S rg;l osr.f :6;.] :;"lf osr5 :0119 .r*5'r.**,,i"J lGl*GAbstractIntroduction: Apelin receptor expressed on the surface ofheart, lung, kidney and other cellsthat have a role in blood pressure regulation and angiogenesis. Leptin is a hormone thalproduced by adipocyte and regulates energy balance by adjusts appetite. The aim of thepresent study was to evaluate four SNPs of Apelin (GzlzA, A445C) and Leptin(223A>C)Genes receptors and leptin( G-2548A) gene in patients with atherosclerosis andhigh blood pressure.Material and methods: This case-control study was carriecl out ou 286 coronary arterydisease (CAD) suspected patients. The participants were divided into 4 subgroups including;CAD patients with no hypertension (H-A', n=61), hypertensive patients with no CAD (H'A-,n=60), cAD patients with hypertensive (H*An, n:95) and non-hypertensive non-CADsubjects as control goup (H A-, n:70). Cenomic DNA from whole blood was extracted andfour SNPs (rsll37l0l rs948847 rc11544374 rs7799A3\ were assessed by PCR-RFLp.Hardy-Weirrberg equilibrium for each polymorphism and nrultinomial logistic. regression wasperformed to evaluate roles of genotypes against hypertension and cAD risk.Results: A significant differences was showed in the genotype frequency of rsl I 544374 inH*A+and CAD group compared to control subjects (P:0.00, P:0.00 respectively). [n the caseof rsl I37l0l SNP, the prevalence of A allele compare to G allele were significantly differentbetween four groups (P:0.02). Results of multinomial regression analysis indicated thatrs11544374 SNP, the recessive genetic model (AA vs. AG+CC) showed GG gelotype wasmeaningfully protective against CAD after (OR= 0.lZ;95% CI : 0.02-0.61; p : 0.01)adjustment, and protective against H+A+after (OR= 0.40; gS% Cl = 0.17-{.98; p = 0.04)adjustment.Conclusion: We conclude that G2.12A rsl1544374 apelin receptor polymorphism has beenprotective effect on CAD, while the allele A of rsl l37l0l potymorphism may be consideredas a hypertensive agent with CAD.Key words: Apelin rec.eptor. Coronary artery disease, Hypertension, Leptin, Polymorphism.SNP'"'...'..........,3,,1,!.,.,..,'.,........*/.:,,,,,**'.*;*y9"Jtu -**l; Alr_l* 31 6.At u.Lz;sya',t'f &r,t*euttC,l.tt sPQtl,,,*rlWsln-1t1 " Jtr* ;*; rt-iar*X d..:r JrF-:'j ,5s:uo;-a)dLt jL-*; *; itt-\ t4t* t)*6')*;? alrl>6it?r;o{;(6111A,&,Aaiu;*,t,5t,,aox;f 6**3sJ-*]1ri*S-;5*d:t*,,*,g*l"tY,lll1 Er a*tV ;y \, *** ri'\\r"*t*:ut;ilfuilil c;l*A:4t*9*,atsJ6at\t1t48et| Ji*;iiltrJ*tr*"Sb,;:/ ;; 4h ,,:, - - \3\ t.Y.**-,, l **-,*-*' dt e1r '. -- u iv u. -r*.::t y : +,g )g*;t'tttli, ;li 3 SUUli L;rtt r";--1:*r1t;t t1.t*llby\i {* *{rl}r,al; 2*7";;:t s :t;J |*dtrw*;tlt,9131 -:*,S:A *t":r." ,;{:4\*;lf *e-:u'*)"JCYi e, f :6\il ;t;> 1r,;':l Jt j,fu aQ. ;;i, zlJl".;v.:.fi.r *; {:;$l *.rtr 1 u*;'*i ;l;1ts tt1, /*;;t.r. ltt:111tt 3t* ln:S'spr.*f,s\r;v:-l9'.5rLl ;.

بررسی ارتباط پلی مورفیسم های تک نوکلوتیدی ژن های گیرنده های اپلین ( G۲۱۲A, A۴۴۵C ) و لپتین ( ۲۲۳AG ) و ژن لپتین ( G-۲۵۴۸A )  با استعداد ابتلا به بیماری های آترواسکلروز و فشار خون بالا

http://eprints.kmu.ac.ir/28047/1/6559_20180724_0001.pdf

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