糖尿病慢传输运动结肠Cajal间质细胞和干细胞因子的变化

cdk1

罗 云, 林 琳, 张红杰, 李学良, 吴高珏, 王美峰1 ]/ v9 |4 m7 K3 R4 ^
罗云, 林琳, 张红杰, 李学良, 吴高珏, 王美峰, 南京医科大学
5 ]: m- \4 k4 w) w& \9 l6 k4 [# _第一附属医院消化内科 江苏省南京市 210029
2 _& [2 K6 K7 X$ X. P) ?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. y' A4 w& E# ]1 \# @
疾病.0 I' j4 C# j3 ?; h4 u+ e
江苏省“135工程”重点人才基金项目, No. RC2003087
* K) `6 |, m( W0 r/ b- D, s江苏省自然科学基金项目, No. BK20041587 J- k$ I. T& }6 `
通讯作者: 林琳, 210029, 江苏省南京市, 南京医科大学第一附( l" Z" v) q& o! m
属医院消化内科. lin9100@yahoo.com.cn
1 y5 w8 p) J9 K* R* t, ~: K8 ?' l电话: 025-83781836-6920
: _% o$ i+ i" z+ n& r' K收稿日期: 2006-11-29 接受日期: 2006-12-18! }7 r$ v& N+ `  r6 Q6 N' U0 R4 Q$ O' d
Alteration of Cajal interstitial) [$ R3 d1 m6 x+ d
cells and stem cell factors in& J3 z3 f. a' S5 v+ f
colon with slow transit motility
. s/ N. c3 _: G" l- N4 y  a# J1 _( Kof diabetes mellitus
* o8 ?; M# x; b' O) lYun Luo, Lin Lin, Hong-Jie Zhang, Xue-Liang Li,9 F, F5 |5 E# W1 e7 O
Gao-Jue Wu, Mei-Feng Wang
- |# Q' v5 S4 J, XYun Luo, Lin Lin, Hong-Jie Zhang, Xue-Liang Li, Gao-
+ }& x9 _3 i6 i/ |+ r8 dJue Wu, Mei-Feng Wang, Department of Gastroenterology,
! t  ?- k  S" g0 d0 V/ i$ V! F; Wthe First Affiliated Hospital of Nanjing Medical University,3 F% x1 Q5 g6 }& S2 D1 U3 g2 P
Nanjing 210029, Jiangsu Province, China
& Z/ H6 I# |% Y9 ^8 l3 ASupported by the Natural Science Foundation of Jiangsu) A- a) L8 J: j: `- u
Province, No. BK2004158, and the Fund from “135 Project”
! F. s- k8 B, c' p3 f, Y2 s& \for the Key Talents of Health and Science Education
. A9 c* h4 z0 I) iDepartment of Jiangsu Province, No. RC2003087
# Q& M+ h- T# ?' B" l- HCorrespondence to: Lin Lin, Department of Gastroenterology,
5 d  a  w& o3 K4 Y3 tthe First Affiliated Hospital of Nanjing Medical; G9 {  g* Z0 o! J
University, Nanjing 210029, Jiangsu Province,
5 }/ e0 X7 x8 n( N7 O: RChina. lin9100@yahoo.com.cn$ T: i& O" P( b$ j+ ^2 G! A
Received: 2006-11-29 Accepted: 2006-12-18
2 g- b2 a; A' l8 r& NAbstract
9 D9 x7 v, y5 f( ^8 ~' bAIM: To observe the alterations of interstitial  ^1 {0 k4 [7 }6 [1 R& [  i$ U- C0 m
cells of Cajal (ICC) and stem cell factors (SCF)
# Z1 ?- P; g/ x2 F) l2 Fin colon tissues with slow transit motility of8 r* |- q+ a6 x: a# {% ?
diabetes mellitus, and study their roles and
( I$ t4 ]% a" F5 B  a+ Xpossible regulatory mechanism.( B: ^/ T6 h8 {
METHODS: A total of 54 male Sprague-Dawley) \+ o  p& w  Z: T+ r4 u
rats were randomly and averagely divided into$ I4 y4 _9 f, v
diabetes group and control group. Diabetes9 \! M  @; ?8 F
model was induced by intraperitoneal injection
# C4 O& |) P$ }2 z, D7 Kof streptozotocin. Nine rats of the above( X5 m3 s. ~- E! W. \1 y- P
two groups were killed respectively 6, 8 and 10, G( r, `# g( @9 e- \% r4 O
weeks after injection. The alterations of ICC and/ v# u7 a# F4 B9 h/ L: O
membrane-bound SCF (M-SCF) in the proximal+ G% V( F3 M/ G7 O
colon tissues were analyzed by immunohistochemistry,& T. ?& S: ]: O5 Z' `- `. w) ^6 R6 U
transmission electron microscopy and" _! _/ X/ x# g0 j
Western blot, and the serum concentration of
4 i' {* Y1 H. xsoluble SCF (S-SCF) were examined by enzymelinked
" V' F+ f8 Y# Q8 Z' w8 bimmunosorbent assay (ELISA).6 C: y; i) E& k9 B: c
RESULTS: The level of blood glucose was elevated* w4 l+ [2 @/ @$ q7 d( y$ v$ H
while the intestinal propulsive rate was
1 g1 T9 E3 `; k4 d1 c" Klowered with the prolonging of time (P > 0.05).; a% k# e; \; e8 \, L) A4 I
Immunohistochemistry showed that the number+ h$ C  M% B0 G6 a" E; h
of myenteric ICC was significantly higher
, L* f8 Q$ w. H6 b  kin diabetic rats than that in the controls, and the
, w3 n  P2 C3 _' dexpression of proximal colon ICC was decreased
1 h9 c7 ~6 l$ a) m! J8 U5 \with the time prolonging. Electron microscopy1 e% n9 B* q4 z  K0 p4 u
exhibited damaged microstructures of colonic+ L( K+ K3 A) v5 [, }# g
ICC such as swelling, vacuole-like degeneration- q; H- i4 n8 ^& e, O
of mitochondria and obvious decrease of+ }: ]2 `0 w% Y- v) F& o
organelles. Meanwhile, the serum concentration' W8 e! e% u/ @8 K! o0 p( [
of S-SCF was remarkably lower in diabetic rats
2 R4 M+ y; _0 B3 \than that in the controls (6 wk: 0.93 ± 0.53 μg/L: o2 N  L5 n) i
vs 1.87 ± 0.92 μg/L, P < 0.05; 8 wk: 0.78 ± 0.21 μg/L
; }( r+ |9 i$ s. i/ k* _vs 1.76 ± 0.94 μg/L, P < 0.05; 10 wk: 0.73 ± 0.20 μg/L* \$ i+ \, {' h
vs 1.82 ± 0.96 μg/L, P < 0.05), but the content of0 ~0 t) U9 O3 n
M-SCF in the colon tissues had no significant
1 Z2 ]5 f0 I9 y/ o2 d9 wdifference between the diabetic and normal rats
  k5 |/ a" Z, X- F(P > 0.05). The alteration trend of S-SCF concentration
; u5 {3 v+ J8 G3 f; l- Z9 [. g0 twas in accordance with that of ICC numbers.2 c2 t- F0 n9 m+ f# t0 A$ B* _3 a
CONCLUSION: Decrease of colonic ICC quantity
/ o" I6 t, p' |) X& Q: F+ M7 I: qand serum S-SCF concentration, and damaged% A3 ?& x8 q6 m
microstructures of ICC are demonstrated in
- F8 [  p& _; S6 }( t3 F' ]7 g1 }' @( mdiabetic rats with slow transit motility of colon,
0 K0 {8 g7 I% @: F8 k. iand these changes and their successive regulation
3 M8 o3 z( u* r9 ]0 E- B) emay contribute to the pathogenesis of slow
$ b: x- R9 Z) K% T1 E, u& Utransit motility.
7 e7 r  P& I* ]1 a" Z% vKey Words: Interstitial cells of Cajal; Stem cell factor;& E2 i3 [  F0 t/ J% w5 n: G+ Z
Colon with slow transit motion; Diabetes mellitus
/ y# ?2 C2 `3 q1 l8 O- vLuo Y, Lin L, Zhang HJ, Li XL, Wu GJ, Wang MF.4 g' e* H/ l  {3 r
Alteration of Cajal interstitial cells and stem cell factors in3 i' }/ a9 X- a$ F7 E* e. H
colon with slow transit motility of diabetes mellitus. Shijie
) g6 Q( _; b( y  V* @! lHuaren Xiaohua Zazhi 2007;15(5):458-463, @- Z- B3 o) {( X* h& e
摘要
7 Y& {6 S7 S1 e) W目的: 了解Cajal间质细胞(ICC)、干细胞因子0 t: z. ?0 Y9 z' a
(SCF)在糖尿病大鼠结肠慢传输运动模型中的: [$ h4 E1 g0 t
变化, 探讨其作用及可能的调控机制.
2 @7 F, e3 p! u方法: 54只♂SD大鼠分为糖尿病和正常对照5 x4 w% {' @8 j4 M6 j$ M
组, 经腹腔注射链脲佐菌素建立糖尿病大鼠! U& [! c2 |- Z8 F2 w& I9 o
模型, 于造模后6, 8, 10 wk各组分别处死9只大
6 G. n* q7 U: |9 r鼠, 以免疫组化、透射电镜研究近端结肠组
! i: d! ?0 J3 n) V织中ICC的变化, 以Western blot方法检测近端: N8 O# R( y& J8 P# O3 k  W) }2 v
结肠组织中膜结合型干细胞因子的表达, 以. X8 {- D5 q) B
ELISA测定血清中可溶型SCF的浓度, 分析他5 `- p0 O, ^8 C7 D8 h5 X. z; n
们之间的相关性.' x8 Q1 D7 z: R9 u# _
结果: 糖尿病大鼠血糖随时间增加而升高, 而0 v. p' u$ O' M
胃肠推进率却降低(P >0.05). 免疫组化结果显# I7 A; A% u( U8 |' E9 g
示, 6, 8, 10 wk时的糖尿病大鼠肌间ICC表达3 t$ q  ~* Y/ N2 [1 s5 G) p3 _* {
较对照组明显减少(P <0.05), 且糖尿病大鼠近& q& s2 ?& _+ R+ o; c
端结肠ICC数量随时间推移有逐渐降少的趋7 u; J* t& F7 V8 W5 X8 a% \/ B0 [$ H
势. 透射电镜显示糖尿病大鼠结肠ICC线粒体+ p& F/ m$ ?" D
肿胀、空泡样变, 细胞器数量明显减少. 与对
0 n  R* a; x6 z6 A/ V% z. Z照组相比, 糖尿病大鼠血清中可溶型SCF显著# \9 U6 g6 T+ H* N
降低(6 wk: 0.93±0.53 μg/L vs 1.87±0.92 μg/1 x/ p- j; c5 \0 D& `1 f+ n" N6 h
L, P <0.05; 8 wk: 0.78±0.21 μg/L vs 1.76±
6 f2 j0 H# U$ M0.94 μg/L, P <0.05; 10 wk: 0.73±0.20 μg/L vs6 g- b3 j; n. K) i" N, h) B
1.82±0.96 μg/L, P <0.05), 而结肠组织中的膜" e8 c' J- \3 m1 d6 ~
结合型SCF无明显差异(P >0.05), 且可溶型干
4 w, {0 U7 M4 k细胞因子与ICC具有相同的变化趋势.
3 @4 q! ^% r! T# y) n结论: 糖尿病胃肠动力障碍大鼠存在血清中
# C6 X4 {/ k) e5 R2 ?* P可溶性干细胞因子浓度下降以及结肠组织中
" }* }' [5 O, o" PICC数量减少和结构破坏, 这些变化及其可能
' K; [+ U( b6 c  E存在的序贯性调控作用可能是糖尿病出现结& ^9 F# o2 E2 ^1 z9 W3 _1 E
肠慢传输变化的基础.- E: a+ \2 D7 y4 L/ _7 S, t8 m) x, i9 E
关键词: 干细胞因子; 糖尿病; 结肠慢传输运动;
5 @- ]) K; f# CCajal间质细胞
0 [  {1 N( R! v罗云, 林琳, 张红杰, 李学良, 吴高珏, 王美峰. 糖尿病慢传输运: @" s) W7 q/ i! p; u( 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
; [5 }% `! L, O2007;15(5):458-463& Z; `. [" |0 G* ^, B% n5 j8 O

% R# {5 z5 {, m5 x+ ]: ]  Z附件是pdf全文。感谢大家支持，回复本贴就可以下载了
3 B. K% h6 c; y8 {  D5 L6 [% c# P7 Y+ B
[hide][/hide]

shihuijunm

谢谢分享

my4321000

回复本贴就可以下载了