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
2 k! e* f0 i* \, Y- e( i1 B罗云, 林琳, 张红杰, 李学良, 吴高珏, 王美峰, 南京医科大学
  [% N. n& i; B5 P. j( z第一附属医院消化内科 江苏省南京市 210029
$ }1 Q7 b4 e# ?9 h! d- J# _( K# v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
2 N) \7 C/ M! Y  |, ]% }* n" p疾病.! F$ k* v* u0 \2 c
江苏省“135工程”重点人才基金项目, No. RC2003087
7 e; [0 T4 c% F4 h+ u: x. p* A: t江苏省自然科学基金项目, No. BK2004158
5 M0 V! l& \- u: Y6 g( U# s通讯作者: 林琳, 210029, 江苏省南京市, 南京医科大学第一附
" y& y0 V2 l1 J$ F属医院消化内科. lin9100@yahoo.com.cn
( A* U3 m1 X3 @2 S, a3 p$ J电话: 025-83781836-6920
6 \9 Q* Q/ R* _+ m5 J: h收稿日期: 2006-11-29 接受日期: 2006-12-18
" Z" z% ]+ b& u% v6 JAlteration of Cajal interstitial2 D% p/ u2 Q2 q
cells and stem cell factors in) K0 K+ o- m7 d* M% d7 }% j# j
colon with slow transit motility7 r0 Y  _) A1 l0 V" J4 R# r( @* J
of diabetes mellitus
1 o9 C. i; U  X6 b( IYun Luo, Lin Lin, Hong-Jie Zhang, Xue-Liang Li,5 c* Q4 f. L6 y3 S
Gao-Jue Wu, Mei-Feng Wang- b, l, q3 a/ F3 @; m) |$ m) Z
Yun Luo, Lin Lin, Hong-Jie Zhang, Xue-Liang Li, Gao-" F2 g7 r3 ]8 d# G7 Z8 @
Jue Wu, Mei-Feng Wang, Department of Gastroenterology,# F. {1 e# f, |2 Z+ O: A2 U
the First Affiliated Hospital of Nanjing Medical University,& }2 k: O+ g4 O
Nanjing 210029, Jiangsu Province, China
: U% }8 w7 f0 P. r$ c( A, l7 nSupported by the Natural Science Foundation of Jiangsu
; N2 m& m% V5 B, b6 I7 \Province, No. BK2004158, and the Fund from “135 Project”
* z# ~7 o- N. ^  ]2 f( @/ @for the Key Talents of Health and Science Education+ Y9 O0 D$ _7 P: s+ s' B
Department of Jiangsu Province, No. RC2003087
6 K8 F% D& s/ x1 H; ECorrespondence to: Lin Lin, Department of Gastroenterology,
, ]& o$ @6 C! i1 dthe First Affiliated Hospital of Nanjing Medical
: I* g5 {4 L+ j% m7 q7 yUniversity, Nanjing 210029, Jiangsu Province,
; ~6 j7 k7 x: n* h# \& T1 P' NChina. lin9100@yahoo.com.cn
- M' r8 T2 i& a2 F& X, `0 v: `Received: 2006-11-29 Accepted: 2006-12-18, T" l9 B  E5 ~/ A
Abstract* o: _: b2 |- }) d% R6 v& t
AIM: To observe the alterations of interstitial
4 p" d8 P3 g# p% d3 ~. H% {cells of Cajal (ICC) and stem cell factors (SCF), d; z% L8 ]4 s$ ~( I6 x$ s! X( b
in colon tissues with slow transit motility of
% k4 b6 T/ L& N2 O/ @4 H% h' W7 mdiabetes mellitus, and study their roles and- u2 `+ Z; H; R5 x; }8 f
possible regulatory mechanism.) `2 [/ s# W6 k' p% d4 U7 i
METHODS: A total of 54 male Sprague-Dawley
" F) n8 b" T9 K" S# yrats were randomly and averagely divided into! Y' ?6 W" `0 S9 Q; c. D
diabetes group and control group. Diabetes
; I7 ]. I4 I) {7 i! i. k$ @model was induced by intraperitoneal injection. W/ y9 E# p  n% _5 N4 Z+ n
of streptozotocin. Nine rats of the above
2 f1 ]0 q5 ^* s7 @* c3 |, j# `two groups were killed respectively 6, 8 and 10
# i9 z- e, s4 l3 _7 y" _3 aweeks after injection. The alterations of ICC and$ J; |& t& r, t( g7 R
membrane-bound SCF (M-SCF) in the proximal/ ^7 D3 A, d, Y8 z: H6 I
colon tissues were analyzed by immunohistochemistry,
7 y3 Q# j# A) l6 p. gtransmission electron microscopy and
8 z3 j+ y, y! V3 ~Western blot, and the serum concentration of
5 F0 H5 a8 [& D: M# N2 R; `4 _4 {( Rsoluble SCF (S-SCF) were examined by enzymelinked% {6 C; G/ v- @8 D/ u
immunosorbent assay (ELISA).1 e+ i) O! S+ D# ]2 S" A1 A
RESULTS: The level of blood glucose was elevated6 X4 K. y3 Y" _3 J* a
while the intestinal propulsive rate was
" q8 u: K6 N7 _7 t8 I$ l3 j5 y1 O% A0 Nlowered with the prolonging of time (P > 0.05).
5 L. g* V" `, X( Y3 v" X5 e, G% yImmunohistochemistry showed that the number$ G( s; O9 ?- l' B/ ~# y. V6 p1 t
of myenteric ICC was significantly higher
: H0 a7 Z! x6 n+ r& Z( s" b( r' Cin diabetic rats than that in the controls, and the
( x% w. X4 n4 p+ {expression of proximal colon ICC was decreased
( N: E0 X4 U% C& Mwith the time prolonging. Electron microscopy$ d! g' K. n" i4 A8 F5 L+ F/ T; J6 Y
exhibited damaged microstructures of colonic6 I6 D. u! x" ~1 Q7 i# W! S" A$ _
ICC such as swelling, vacuole-like degeneration
2 ^8 F9 F# v+ K' m& o1 Zof mitochondria and obvious decrease of! e" C+ M4 l; q# U% P/ |; q
organelles. Meanwhile, the serum concentration; H' Z" e7 M: j/ c9 b9 Z! C
of S-SCF was remarkably lower in diabetic rats4 K" r9 G* ~$ x
than that in the controls (6 wk: 0.93 ± 0.53 μg/L9 B1 f( k: S% `4 j5 d2 ]& f$ _
vs 1.87 ± 0.92 μg/L, P < 0.05; 8 wk: 0.78 ± 0.21 μg/L2 c" Y/ a! J5 M1 _2 g7 u1 k, Q
vs 1.76 ± 0.94 μg/L, P < 0.05; 10 wk: 0.73 ± 0.20 μg/L, m6 Z5 X+ a* D6 d
vs 1.82 ± 0.96 μg/L, P < 0.05), but the content of# W- g! }# p& l- B3 m4 z6 ^
M-SCF in the colon tissues had no significant
% b8 P/ ~; N& J4 [- Adifference between the diabetic and normal rats
9 _) T- C7 W% A$ y: a(P > 0.05). The alteration trend of S-SCF concentration4 }" M# g3 l* d* E; ?
was in accordance with that of ICC numbers./ p/ s. }% U  `1 V
CONCLUSION: Decrease of colonic ICC quantity4 {, H$ B& s! G2 n) h! c
and serum S-SCF concentration, and damaged6 _/ Z2 q0 E) Z( t9 _6 o* N- `2 }
microstructures of ICC are demonstrated in
3 I- ?5 [4 W, C3 rdiabetic rats with slow transit motility of colon,) e0 {* b# v0 X+ O0 R
and these changes and their successive regulation/ X. G1 D3 F2 Q  k) \8 F
may contribute to the pathogenesis of slow% e$ t; |, U9 ~, q/ P* [' y5 U. x
transit motility.
1 M9 ]$ H; i& K4 QKey Words: Interstitial cells of Cajal; Stem cell factor;5 s) j) k3 {/ q. ~- q  k" a
Colon with slow transit motion; Diabetes mellitus
+ E, z' L6 b) i2 ~- gLuo Y, Lin L, Zhang HJ, Li XL, Wu GJ, Wang MF.* c; p1 A' E2 ?, \5 G
Alteration of Cajal interstitial cells and stem cell factors in5 H. V# ^! j3 v/ d
colon with slow transit motility of diabetes mellitus. Shijie
. G$ E1 F8 D/ z& @Huaren Xiaohua Zazhi 2007;15(5):458-463
: g/ J8 l5 ?0 J1 S, e摘要, M, L' a7 {$ U7 S8 {) Q
目的: 了解Cajal间质细胞(ICC)、干细胞因子# w; u0 t# P: M2 F6 \2 A3 A2 t: {
(SCF)在糖尿病大鼠结肠慢传输运动模型中的
' G; r& R$ a4 w& \% ~7 ?  w! n变化, 探讨其作用及可能的调控机制.
6 i9 t' |! v2 m4 C3 z, O/ p! S# u方法: 54只♂SD大鼠分为糖尿病和正常对照2 b8 o0 E) {1 j$ v
组, 经腹腔注射链脲佐菌素建立糖尿病大鼠5 i4 [2 l$ t7 `- D, o& W
模型, 于造模后6, 8, 10 wk各组分别处死9只大
5 j% ^/ \3 I- J, T2 `; }鼠, 以免疫组化、透射电镜研究近端结肠组
" t; m3 F4 D9 G1 W# J3 e. P) [0 ]织中ICC的变化, 以Western blot方法检测近端7 i  U+ l( @  [
结肠组织中膜结合型干细胞因子的表达, 以: l' U; I& {0 Q; D/ s) t( i! l
ELISA测定血清中可溶型SCF的浓度, 分析他6 k3 L" L+ q6 q8 v! S
们之间的相关性.
5 p6 b; F+ C! Z* w$ I结果: 糖尿病大鼠血糖随时间增加而升高, 而" F' _' O: H; o: [, h
胃肠推进率却降低(P >0.05). 免疫组化结果显# p& ]0 h5 ~3 o
示, 6, 8, 10 wk时的糖尿病大鼠肌间ICC表达
8 N2 V$ L5 z' N* ^1 m较对照组明显减少(P <0.05), 且糖尿病大鼠近7 V$ J: n( \. I, G
端结肠ICC数量随时间推移有逐渐降少的趋
% y% C% n) I( a势. 透射电镜显示糖尿病大鼠结肠ICC线粒体
1 M& n" W5 _. O5 ]  e+ V' o: w肿胀、空泡样变, 细胞器数量明显减少. 与对" E1 j5 V+ L8 k# Q$ q
照组相比, 糖尿病大鼠血清中可溶型SCF显著
; Z$ V" q" D( |, |6 @% e0 W降低(6 wk: 0.93±0.53 μg/L vs 1.87±0.92 μg/
; _2 t( V6 H4 @: ]) e( L. ?- UL, P <0.05; 8 wk: 0.78±0.21 μg/L vs 1.76±1 s9 e; t  u& E& ~8 f! L/ d
0.94 μg/L, P <0.05; 10 wk: 0.73±0.20 μg/L vs+ o! h! l5 T; |/ p, j6 h
1.82±0.96 μg/L, P <0.05), 而结肠组织中的膜
5 D! I& A8 e! \. X- h, z8 z: H) ]结合型SCF无明显差异(P >0.05), 且可溶型干5 z0 E4 I4 e/ a3 f  {+ ?
细胞因子与ICC具有相同的变化趋势.9 f. z+ r- f: P0 a# e" W% \! }% j, D# w
结论: 糖尿病胃肠动力障碍大鼠存在血清中% p: @$ P& T, J. B% W% E
可溶性干细胞因子浓度下降以及结肠组织中# \1 }. p" I" @5 A# o
ICC数量减少和结构破坏, 这些变化及其可能
; T0 ~0 `7 H! m2 @2 Y存在的序贯性调控作用可能是糖尿病出现结
2 L4 @. T9 |6 `. V3 V; _2 ?肠慢传输变化的基础.; s. z3 c! P' M
关键词: 干细胞因子; 糖尿病; 结肠慢传输运动;( g( B6 I& G: d& \, Z- u7 _
Cajal间质细胞) b) o- m+ S  h& k- l* G
罗云, 林琳, 张红杰, 李学良, 吴高珏, 王美峰. 糖尿病慢传输运$ ~4 K4 S2 `' S! T& i! i6 z
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
4 V2 }2 X- K% p3 X8 X2007;15(5):458-4638 m$ R7 n. t5 i! |9 i1 w

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