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
' B0 ~; F- l8 n5 s- B; r6 f罗云, 林琳, 张红杰, 李学良, 吴高珏, 王美峰, 南京医科大学- T$ L3 k1 V4 x' ]( o2 D& U9 Z5 r
第一附属医院消化内科 江苏省南京市 210029
, Z2 G- A* q. I) W2 @8 w$ A+ A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, h( k7 M! S5 R5 N5 g/ w
疾病.
7 P- l' M/ b# x( Z江苏省“135工程”重点人才基金项目, No. RC2003087
) }9 D, S- h" u4 [/ r江苏省自然科学基金项目, No. BK2004158- C" c; a7 h: A. R; n# g
通讯作者: 林琳, 210029, 江苏省南京市, 南京医科大学第一附
& h1 A' w$ M5 t2 G/ Q属医院消化内科. lin9100@yahoo.com.cn
6 x4 k9 r. e+ w! z1 F电话: 025-83781836-6920
' i) e7 w& T- @  r3 M收稿日期: 2006-11-29 接受日期: 2006-12-18
" z, w. b* i; z8 c/ {Alteration of Cajal interstitial3 h! c& s, S5 z% D, s
cells and stem cell factors in
+ w" P2 p! |9 ^6 Scolon with slow transit motility
4 l' j7 @9 q5 m+ Y2 d' W) hof diabetes mellitus
' |9 s, a9 M0 A$ M* S6 J) EYun Luo, Lin Lin, Hong-Jie Zhang, Xue-Liang Li,9 ]9 v' M# b& U& q' s
Gao-Jue Wu, Mei-Feng Wang
& ^9 r6 {' Y' F$ V* [Yun Luo, Lin Lin, Hong-Jie Zhang, Xue-Liang Li, Gao-
" k3 j" h- q+ u+ d/ ?' U' hJue Wu, Mei-Feng Wang, Department of Gastroenterology,
/ |/ \: ]' P# w/ N1 dthe First Affiliated Hospital of Nanjing Medical University,
/ H6 ?7 T, k" G5 s- d" s7 XNanjing 210029, Jiangsu Province, China
- J# X! `. Q7 h  ~Supported by the Natural Science Foundation of Jiangsu. f& O3 f7 f) `% A5 Z" r
Province, No. BK2004158, and the Fund from “135 Project”
& q  g6 R: N# t8 m: c! yfor the Key Talents of Health and Science Education
; X' X# a6 p2 @0 Y4 e3 [Department of Jiangsu Province, No. RC20030878 \  ~; v$ ?& S1 D- m
Correspondence to: Lin Lin, Department of Gastroenterology,
, J: b$ K4 f9 X6 G4 z7 }- ~8 {/ c" @the First Affiliated Hospital of Nanjing Medical4 T2 R! c1 i( l9 M9 n& @
University, Nanjing 210029, Jiangsu Province,
/ ^6 I1 }6 i/ b2 \China. lin9100@yahoo.com.cn
4 \4 c$ t9 m# N* |6 C( ], _Received: 2006-11-29 Accepted: 2006-12-18
5 v2 P9 x/ G2 [9 g; }Abstract
- |. K9 N8 s3 VAIM: To observe the alterations of interstitial
# W7 g$ u* t5 i' ~1 q$ k$ C! \2 zcells of Cajal (ICC) and stem cell factors (SCF)' G0 l( ]! M' ~( I/ }
in colon tissues with slow transit motility of
( s; M$ ?0 n7 H* |diabetes mellitus, and study their roles and
; W, t. q% l- k6 a1 C; opossible regulatory mechanism.
( {4 h* t4 A7 s( K4 rMETHODS: A total of 54 male Sprague-Dawley# w+ _( y; F2 F, ?! r4 v. A
rats were randomly and averagely divided into9 _  y8 ?' r9 L6 U
diabetes group and control group. Diabetes
  A, B. l5 O2 pmodel was induced by intraperitoneal injection, A& V- n& C( P6 g
of streptozotocin. Nine rats of the above& |+ M5 \: K' E2 G, J8 K
two groups were killed respectively 6, 8 and 10; W3 |# e7 n/ v3 _5 o* x+ E) ?
weeks after injection. The alterations of ICC and$ t* w% u+ j2 Q+ r) F% Z
membrane-bound SCF (M-SCF) in the proximal0 G8 i% c$ J* t8 o9 w- P4 a( v$ P' a
colon tissues were analyzed by immunohistochemistry,4 i0 s' U+ U; d& W
transmission electron microscopy and
# y5 S( ?" u  i6 X2 a" uWestern blot, and the serum concentration of8 K( \# W0 E0 n2 W
soluble SCF (S-SCF) were examined by enzymelinked
$ l9 p* q& L0 p, Iimmunosorbent assay (ELISA).
/ g: D; z/ K# m7 ]2 h3 FRESULTS: The level of blood glucose was elevated5 B2 B4 s" f9 u4 b9 `
while the intestinal propulsive rate was
$ L$ e0 ~# m  m7 `9 P+ J! c. Tlowered with the prolonging of time (P > 0.05).  K9 f/ C' Z* I8 Z! w. x+ z
Immunohistochemistry showed that the number) \  C) i  ^- E$ C8 S8 E# O
of myenteric ICC was significantly higher4 z( P' ~+ c4 I% H- C+ S, `
in diabetic rats than that in the controls, and the
  c+ k# D$ A: z" f& ]" a0 yexpression of proximal colon ICC was decreased) l! W/ A3 N5 H
with the time prolonging. Electron microscopy" b% b; J( G4 S, F
exhibited damaged microstructures of colonic
! P) e) ?. v% {: l+ HICC such as swelling, vacuole-like degeneration
5 Q' F6 O% \& s2 p) [of mitochondria and obvious decrease of9 E5 ^6 G6 w; ~5 o  S- }
organelles. Meanwhile, the serum concentration
7 u, [; j& k: Z$ Y; V' d. Z& Pof S-SCF was remarkably lower in diabetic rats
& I1 c$ Q' ~+ Ythan that in the controls (6 wk: 0.93 ± 0.53 μg/L
3 B+ k8 E  Q0 |vs 1.87 ± 0.92 μg/L, P < 0.05; 8 wk: 0.78 ± 0.21 μg/L4 i  H7 a6 ^- t' P7 q
vs 1.76 ± 0.94 μg/L, P < 0.05; 10 wk: 0.73 ± 0.20 μg/L" ~9 T1 l& Y+ y0 Y0 ^5 Y
vs 1.82 ± 0.96 μg/L, P < 0.05), but the content of
  ?& o0 u. Q  {8 |! lM-SCF in the colon tissues had no significant3 A0 I8 H$ j$ l$ a2 Q
difference between the diabetic and normal rats
" h9 M+ {- c- }9 N(P > 0.05). The alteration trend of S-SCF concentration8 `$ X  x/ O( X1 `; @
was in accordance with that of ICC numbers.' E% \$ x+ l- ]) [! [' W
CONCLUSION: Decrease of colonic ICC quantity
4 _( I- I, L  U; x( s% }) nand serum S-SCF concentration, and damaged
, ?5 f1 u1 ~# a, C7 umicrostructures of ICC are demonstrated in0 H  X. B6 g& B2 a/ b+ {
diabetic rats with slow transit motility of colon,' d& R' r3 K7 \% r5 s3 s, L- {
and these changes and their successive regulation
# ^7 f& K% ?8 P  F* f- nmay contribute to the pathogenesis of slow- l, w! ~# k) E2 \" X! p
transit motility.3 ]. |% {/ ~/ l4 m
Key Words: Interstitial cells of Cajal; Stem cell factor;8 p& r* J7 V7 V0 x  ]
Colon with slow transit motion; Diabetes mellitus6 o- y+ _, g* b6 N5 E( g
Luo Y, Lin L, Zhang HJ, Li XL, Wu GJ, Wang MF.
, j# ]* A, i3 q' ^6 ~0 K* ZAlteration of Cajal interstitial cells and stem cell factors in
# E4 j3 |9 z8 z' S3 |colon with slow transit motility of diabetes mellitus. Shijie' X3 |+ K$ c/ `3 i
Huaren Xiaohua Zazhi 2007;15(5):458-463
6 F% P, r; S3 ^% f. b: Y5 ]摘要
! f) F9 z4 x7 h3 v3 m) \0 k目的: 了解Cajal间质细胞(ICC)、干细胞因子9 k( D2 m( T  _/ N& T
(SCF)在糖尿病大鼠结肠慢传输运动模型中的
- B5 \+ O0 G, e' `6 O( l4 t' g变化, 探讨其作用及可能的调控机制.
  i+ ^1 X# g2 d8 ?' n1 T方法: 54只♂SD大鼠分为糖尿病和正常对照3 e( w- q) i9 g4 ~
组, 经腹腔注射链脲佐菌素建立糖尿病大鼠1 [6 \! v+ z; \& X
模型, 于造模后6, 8, 10 wk各组分别处死9只大
& B/ e' Y5 N' Z7 ]鼠, 以免疫组化、透射电镜研究近端结肠组
$ y4 U, m" ]; q织中ICC的变化, 以Western blot方法检测近端4 h& {0 c& S# s
结肠组织中膜结合型干细胞因子的表达, 以+ L8 Y& p  k% |& C
ELISA测定血清中可溶型SCF的浓度, 分析他# ]6 p; [+ r1 R5 C6 Q2 s& \
们之间的相关性.) K: x9 F5 R, s" H
结果: 糖尿病大鼠血糖随时间增加而升高, 而
% u1 K" z5 [$ K! g" R胃肠推进率却降低(P >0.05). 免疫组化结果显0 }: T# Q8 d% I6 y/ o6 n
示, 6, 8, 10 wk时的糖尿病大鼠肌间ICC表达
. v8 C) R6 [1 ?5 \较对照组明显减少(P <0.05), 且糖尿病大鼠近9 T6 I( o- y/ H% o* R
端结肠ICC数量随时间推移有逐渐降少的趋( d) s: c! I7 q  d9 ?* p
势. 透射电镜显示糖尿病大鼠结肠ICC线粒体" ?% X" Z9 ^$ K$ K! H5 N8 M
肿胀、空泡样变, 细胞器数量明显减少. 与对+ W' T' [8 g, y/ Y
照组相比, 糖尿病大鼠血清中可溶型SCF显著1 l5 x! U9 y; X/ I# w! k3 z
降低(6 wk: 0.93±0.53 μg/L vs 1.87±0.92 μg/; }7 I) k9 _% {
L, P <0.05; 8 wk: 0.78±0.21 μg/L vs 1.76±
  X5 O% X% e1 X5 @" L5 ^) P0.94 μg/L, P <0.05; 10 wk: 0.73±0.20 μg/L vs: a7 R% \% c" o/ L7 K3 P# L
1.82±0.96 μg/L, P <0.05), 而结肠组织中的膜
+ c: R6 X/ \, ?6 ^8 w: p. K结合型SCF无明显差异(P >0.05), 且可溶型干
- {& P8 z  k1 [" F2 ?细胞因子与ICC具有相同的变化趋势.) Q: O7 A5 |) B
结论: 糖尿病胃肠动力障碍大鼠存在血清中' s# z7 P1 Q) i0 [1 r# P: K( @; ?
可溶性干细胞因子浓度下降以及结肠组织中% D2 y; J2 d0 `8 y4 I, _
ICC数量减少和结构破坏, 这些变化及其可能3 N$ K7 u8 u7 r0 u' a
存在的序贯性调控作用可能是糖尿病出现结2 {. ~7 \' ~' k* ]$ z( T  t
肠慢传输变化的基础.
# ?6 m- j; z: w关键词: 干细胞因子; 糖尿病; 结肠慢传输运动;7 ?- d7 P: U* v" \% d
Cajal间质细胞
) z" x. d1 f- G* Z罗云, 林琳, 张红杰, 李学良, 吴高珏, 王美峰. 糖尿病慢传输运
! l4 }. L8 v# n7 V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
( U/ W0 m( F/ h' v8 Z6 j; \2 G6 A9 ]: B- J2007;15(5):458-463
' O) p1 W& @! \  i$ {. @
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