糖尿病慢传输运动结肠Cajal间质细胞和干细胞因子的变化

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罗 云, 林 琳, 张红杰, 李学良, 吴高珏, 王美峰  `) v8 _! r; m( ]5 L
罗云, 林琳, 张红杰, 李学良, 吴高珏, 王美峰, 南京医科大学4 j* F$ Q: i0 ?) O7 D
第一附属医院消化内科 江苏省南京市 2100293 Y, T* v8 c! O6 a1 M
罗云, 南京医科大学硕士研究生, 主要研究方向为胃肠动力性4 N% n' w0 Q! t4 I& Z( K0 r" i) x
疾病.3 b1 i, W3 _# _  g
江苏省“135工程”重点人才基金项目, No. RC20030870 K4 U2 f# E5 V  ]/ p: `/ U+ D2 Q
江苏省自然科学基金项目, No. BK2004158
' J6 f* G% C. O. P通讯作者: 林琳, 210029, 江苏省南京市, 南京医科大学第一附# [- K! d, h! Y5 H' i  A+ a
属医院消化内科. lin9100@yahoo.com.cn4 ^: [3 y* C8 _8 J
电话: 025-83781836-6920
5 [) B0 ^/ G# w; _, V, z收稿日期: 2006-11-29 接受日期: 2006-12-18  x) @7 Z% y2 R( _5 a! M
Alteration of Cajal interstitial/ N% E5 X) Q5 j; ~; Q
cells and stem cell factors in# L/ g/ g) I) q% d4 T8 ~
colon with slow transit motility
, ]" z# \2 i6 H/ d  ~  Wof diabetes mellitus
1 i3 u, e1 t1 a, B7 b$ t' pYun Luo, Lin Lin, Hong-Jie Zhang, Xue-Liang Li,
" Y. B5 w2 k( ?, S# o0 v3 T. OGao-Jue Wu, Mei-Feng Wang
: p2 ~* G# v2 ]: z( K/ UYun Luo, Lin Lin, Hong-Jie Zhang, Xue-Liang Li, Gao-
8 [( O' f9 d' n' X1 dJue Wu, Mei-Feng Wang, Department of Gastroenterology,6 y/ o0 L4 S) r! ]! C. W
the First Affiliated Hospital of Nanjing Medical University,8 u  I3 }( k8 \9 {" g0 J. K+ J
Nanjing 210029, Jiangsu Province, China3 Y5 Q# [: \( R, x
Supported by the Natural Science Foundation of Jiangsu, _' j4 V/ |* ?5 W8 L7 L1 l: d
Province, No. BK2004158, and the Fund from “135 Project”" ~; E" J; B3 U" ~2 U5 e, w
for the Key Talents of Health and Science Education
( _( L3 o! T/ @( S3 x8 y- b. hDepartment of Jiangsu Province, No. RC20030878 c! V- Z: N- |8 T( M: g
Correspondence to: Lin Lin, Department of Gastroenterology,
; P$ y9 F# O8 L( |the First Affiliated Hospital of Nanjing Medical5 q; t0 `' ^$ n2 G3 b2 N2 l
University, Nanjing 210029, Jiangsu Province,# \8 P( m5 b3 c+ D- b+ F  y
China. lin9100@yahoo.com.cn
; W: R/ k2 ^% X# |Received: 2006-11-29 Accepted: 2006-12-18( H% I* t7 J3 v: G. J
Abstract& {# S# y& T" Z
AIM: To observe the alterations of interstitial
; d, c# h& N/ p- Kcells of Cajal (ICC) and stem cell factors (SCF)9 g0 W: }" m5 M' T* l1 q4 l/ u7 p" w% y) p
in colon tissues with slow transit motility of
$ c, J% P$ k7 b7 }% [. f0 t0 k, _diabetes mellitus, and study their roles and' z, K6 L! c/ S+ |
possible regulatory mechanism.& U/ ~7 O! v4 h6 M8 ?% ]
METHODS: A total of 54 male Sprague-Dawley, [2 h5 b$ Z  T& i6 o% [9 U
rats were randomly and averagely divided into
  X; D7 j! b- K! Y7 m4 F" e% U# K0 G  O% jdiabetes group and control group. Diabetes. [& e! e4 N% r9 j7 W1 y
model was induced by intraperitoneal injection" o+ w0 l* U6 U1 S) ?
of streptozotocin. Nine rats of the above
+ }0 G6 C/ U. j* v5 r' o7 w2 Wtwo groups were killed respectively 6, 8 and 10
& a# R$ T4 G- C4 fweeks after injection. The alterations of ICC and
/ W; P: D! S; kmembrane-bound SCF (M-SCF) in the proximal7 u  \/ l) ~( `. t/ c! G
colon tissues were analyzed by immunohistochemistry,
* w/ X2 m( _+ x6 s" m- \1 {6 wtransmission electron microscopy and( G+ `0 u3 y1 q" Z( m; U$ s  C8 w
Western blot, and the serum concentration of
, ?$ H6 ~+ r- Z! [( U( d6 Bsoluble SCF (S-SCF) were examined by enzymelinked
; @0 ^; X* e  G+ Himmunosorbent assay (ELISA).5 v9 W; c4 z6 D- w. _6 Y8 P! s
RESULTS: The level of blood glucose was elevated
( u. m5 V5 @! y2 k+ s' d1 P$ ~: mwhile the intestinal propulsive rate was
4 p) `% i, ~# B1 M+ }# C+ Qlowered with the prolonging of time (P > 0.05).. O4 y8 v9 |- c1 a! k4 v
Immunohistochemistry showed that the number
5 o# U( P6 m& R9 t1 B+ c( M, Kof myenteric ICC was significantly higher
1 X. R- C8 y# C  M5 Q0 ]( Cin diabetic rats than that in the controls, and the8 S: T: ~7 ?0 Z) p' P% t1 J
expression of proximal colon ICC was decreased( M7 W5 [- o4 W! p& _5 R
with the time prolonging. Electron microscopy
4 |4 r% r3 r& _* k- @3 qexhibited damaged microstructures of colonic
* T$ z. j  l0 r8 NICC such as swelling, vacuole-like degeneration
9 L* w' Q3 j1 |of mitochondria and obvious decrease of8 g, x! m" `7 K0 M
organelles. Meanwhile, the serum concentration
% W5 M' ?7 a  D- w6 f3 Bof S-SCF was remarkably lower in diabetic rats% Y8 m- [+ U1 N' K) y
than that in the controls (6 wk: 0.93 ± 0.53 μg/L
) Q; D/ r0 i* ], Tvs 1.87 ± 0.92 μg/L, P < 0.05; 8 wk: 0.78 ± 0.21 μg/L( i  h, r- x6 v9 Z0 D4 Q! n" o
vs 1.76 ± 0.94 μg/L, P < 0.05; 10 wk: 0.73 ± 0.20 μg/L
* X( A% p% L. M) Q: _vs 1.82 ± 0.96 μg/L, P < 0.05), but the content of
$ \3 E& [0 c- s$ v. [9 RM-SCF in the colon tissues had no significant
) ]1 N. d" W, K6 Wdifference between the diabetic and normal rats
8 O( z+ P8 q# g4 X) Q(P > 0.05). The alteration trend of S-SCF concentration# e7 i* P0 S& s6 y" z
was in accordance with that of ICC numbers.
: {* ]4 ^1 b$ g2 o+ E% e3 dCONCLUSION: Decrease of colonic ICC quantity7 i. t, d# ^) g
and serum S-SCF concentration, and damaged
: p- c" C8 ^( e! E" P  Gmicrostructures of ICC are demonstrated in6 l( z& }, d; M
diabetic rats with slow transit motility of colon,1 i# G: h) y8 q9 e; B4 |) x
and these changes and their successive regulation
- f1 V5 q( X2 ~8 Gmay contribute to the pathogenesis of slow
0 j+ @9 E' d  t% E$ h5 _transit motility.
5 @6 D! A6 H6 |  ~7 q" e0 _Key Words: Interstitial cells of Cajal; Stem cell factor;; C; o( p8 U, i- G
Colon with slow transit motion; Diabetes mellitus
2 r1 p4 K" F; H9 k# K/ {Luo Y, Lin L, Zhang HJ, Li XL, Wu GJ, Wang MF.; u7 x+ x6 c. w) Y+ |
Alteration of Cajal interstitial cells and stem cell factors in
% V" o9 Z2 u- L8 y) e1 C# x" jcolon with slow transit motility of diabetes mellitus. Shijie$ {/ y( _5 P" r$ a7 {" l
Huaren Xiaohua Zazhi 2007;15(5):458-463
! v. Q6 a* l, D9 B3 _! [* e摘要1 g* K. o: k' @9 A
目的: 了解Cajal间质细胞(ICC)、干细胞因子/ T' w6 y" m' R- G; w/ I  E
(SCF)在糖尿病大鼠结肠慢传输运动模型中的
, C# k6 c+ U; y6 U4 o变化, 探讨其作用及可能的调控机制.
  N& U( u( r4 e: t+ L方法: 54只♂SD大鼠分为糖尿病和正常对照5 S+ |! x2 b) w3 H) b+ B+ t+ v  {
组, 经腹腔注射链脲佐菌素建立糖尿病大鼠. ~6 ?6 H/ Z" |4 M3 D! H8 G
模型, 于造模后6, 8, 10 wk各组分别处死9只大0 L# P& \& h, @' E
鼠, 以免疫组化、透射电镜研究近端结肠组
' L- L: x. Z! N- f织中ICC的变化, 以Western blot方法检测近端8 X1 t+ N" t5 W4 W) R
结肠组织中膜结合型干细胞因子的表达, 以/ f2 |# o" Z  p2 i" U2 S
ELISA测定血清中可溶型SCF的浓度, 分析他  J/ ~7 J' ?$ `: i7 g
们之间的相关性.
' A. v& L3 \5 G1 b8 v% m, y" w  ?结果: 糖尿病大鼠血糖随时间增加而升高, 而2 p5 |3 p9 N0 h
胃肠推进率却降低(P >0.05). 免疫组化结果显8 e! ~7 ~! j2 j" F. _1 ~8 P$ s
示, 6, 8, 10 wk时的糖尿病大鼠肌间ICC表达; O- P- \; @& J% b4 B
较对照组明显减少(P <0.05), 且糖尿病大鼠近
/ f) q! Y6 H. H2 _' E6 [# d端结肠ICC数量随时间推移有逐渐降少的趋) V! q, c5 W( ~: _
势. 透射电镜显示糖尿病大鼠结肠ICC线粒体0 O0 l; `. d! c+ A0 m! _0 W
肿胀、空泡样变, 细胞器数量明显减少. 与对
9 ^0 a" J. C8 o& S照组相比, 糖尿病大鼠血清中可溶型SCF显著
/ y  K4 T2 A9 Q" @降低(6 wk: 0.93±0.53 μg/L vs 1.87±0.92 μg/+ g! f( X/ `# y7 |% B% \
L, P <0.05; 8 wk: 0.78±0.21 μg/L vs 1.76±
/ g/ e" x5 F7 [6 O. P0.94 μg/L, P <0.05; 10 wk: 0.73±0.20 μg/L vs
  {- _3 q2 p( h1.82±0.96 μg/L, P <0.05), 而结肠组织中的膜
/ R5 }7 o- b" f! @; V2 p9 Z6 \结合型SCF无明显差异(P >0.05), 且可溶型干8 `3 D3 s3 E0 _1 v: h3 Y
细胞因子与ICC具有相同的变化趋势.' v5 H$ c: ]( n7 S' e+ U( B
结论: 糖尿病胃肠动力障碍大鼠存在血清中
( E( t6 L. Z$ @4 P* ^3 Z2 W可溶性干细胞因子浓度下降以及结肠组织中: r4 M, C" B0 S$ T: k9 e
ICC数量减少和结构破坏, 这些变化及其可能
8 f1 S: t! m, Z/ W& z$ \! B! I1 K存在的序贯性调控作用可能是糖尿病出现结
# e+ n4 L' T" ?  [! E# [( L肠慢传输变化的基础.$ ^, K5 y) U# \* ?  x3 P  Y) }, N
关键词: 干细胞因子; 糖尿病; 结肠慢传输运动;
* U! L3 h, j7 }4 Z+ kCajal间质细胞& [0 \+ t* r6 b1 {
罗云, 林琳, 张红杰, 李学良, 吴高珏, 王美峰. 糖尿病慢传输运4 @& X  ]% t) y! n1 d
动结肠Cajal间质细胞和干细胞因子的变化. 世界华人消化杂志
8 K1 g3 n# c) g8 Y2007;15(5):458-463
  q( V! b- k- W* c  x
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