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
7 @( K( H% ^5 z7 `  n- N罗云, 林琳, 张红杰, 李学良, 吴高珏, 王美峰, 南京医科大学' z1 I; B  }8 X
第一附属医院消化内科 江苏省南京市 210029
- ^1 C5 B- B  p+ w& Q! H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, V5 B* w- E( a/ o/ E6 l/ w. e
疾病.% [# C! t5 M# O0 G
江苏省“135工程”重点人才基金项目, No. RC2003087
; p7 p6 ^1 Z8 q, X" t$ M江苏省自然科学基金项目, No. BK2004158( W% D5 a/ p7 ]! C  w# B7 Z
通讯作者: 林琳, 210029, 江苏省南京市, 南京医科大学第一附# [" x8 R" \! i! x* u  L! N5 G
属医院消化内科. lin9100@yahoo.com.cn( F- t' ]% _- [$ R+ U
电话: 025-83781836-6920
4 S4 T: q5 o# B, ?' V4 T+ I  `收稿日期: 2006-11-29 接受日期: 2006-12-18( G4 L5 w7 T& S0 p; N, [5 @5 h
Alteration of Cajal interstitial2 F" b9 L# _) w6 T& B
cells and stem cell factors in
0 S7 X+ t$ S( _colon with slow transit motility
7 s: S( c6 q( r5 `# Vof diabetes mellitus5 y& n) N1 j5 N
Yun Luo, Lin Lin, Hong-Jie Zhang, Xue-Liang Li,
+ J1 C' y5 T8 T/ `7 R" i* |4 SGao-Jue Wu, Mei-Feng Wang
/ ]4 q  M. o% L0 K- L8 yYun Luo, Lin Lin, Hong-Jie Zhang, Xue-Liang Li, Gao-8 ~# L8 r8 A$ k, d* N
Jue Wu, Mei-Feng Wang, Department of Gastroenterology,7 j+ u; V8 K$ M8 i$ J: W
the First Affiliated Hospital of Nanjing Medical University,
- ?2 J; v" @5 @% A) `6 {& FNanjing 210029, Jiangsu Province, China
% g$ ?$ G$ ~. e7 C  l# g  gSupported by the Natural Science Foundation of Jiangsu  y5 W. B; ~3 _$ ^
Province, No. BK2004158, and the Fund from “135 Project”
0 t2 [7 t4 b2 Yfor the Key Talents of Health and Science Education
. B) k/ Z/ D; {5 W7 L$ IDepartment of Jiangsu Province, No. RC2003087
& ]- h. ]: ^, }) Y1 jCorrespondence to: Lin Lin, Department of Gastroenterology,
. U% i$ O4 s4 v( j* Tthe First Affiliated Hospital of Nanjing Medical
- }( f' M" q% g3 L: @University, Nanjing 210029, Jiangsu Province,
. d: e: u5 G2 v1 D* Z1 fChina. lin9100@yahoo.com.cn
) G6 m/ Y- X- ^7 I5 jReceived: 2006-11-29 Accepted: 2006-12-18
8 z6 X2 f: W' a4 w: F/ ^Abstract& [- N, j: w  V4 ?3 y5 H  |
AIM: To observe the alterations of interstitial' b) t1 C: M- e9 m3 h: d& z8 ^
cells of Cajal (ICC) and stem cell factors (SCF)$ s" L. Z# i5 s8 m+ ]
in colon tissues with slow transit motility of0 c' f5 S& n& L
diabetes mellitus, and study their roles and
7 @3 [' m3 V: fpossible regulatory mechanism.& Z! e' A! g, u7 B. q# s+ k/ r
METHODS: A total of 54 male Sprague-Dawley6 n4 [0 N. |; R/ L/ |
rats were randomly and averagely divided into
& q' q4 y* i+ ]" o1 M# g5 @diabetes group and control group. Diabetes
7 B' x# f3 S; _1 v4 E& smodel was induced by intraperitoneal injection
. H: f; K2 b, `! z& ~1 R/ l! ]of streptozotocin. Nine rats of the above$ Z8 d+ h1 n4 F/ Y  ]4 i* Q$ \
two groups were killed respectively 6, 8 and 10
  h: r7 i6 U2 s0 ?. G' b# ?6 y' Dweeks after injection. The alterations of ICC and
) ~6 g7 ?  O( a7 Q! |3 Q3 rmembrane-bound SCF (M-SCF) in the proximal
1 B! Y* ]4 q4 T1 Scolon tissues were analyzed by immunohistochemistry,
4 b2 i6 b& G" J7 `transmission electron microscopy and
7 w7 t6 _0 m6 z7 o5 s, \Western blot, and the serum concentration of
+ w3 x4 x. |! ]9 P* p' q" J+ hsoluble SCF (S-SCF) were examined by enzymelinked
$ x! J1 T% X: p& }) R; qimmunosorbent assay (ELISA).8 V; O' V5 g+ O
RESULTS: The level of blood glucose was elevated+ ^7 {) N0 r) I- e0 Q
while the intestinal propulsive rate was/ p8 R; B7 I; K) y1 B% I: e$ W$ W
lowered with the prolonging of time (P > 0.05).
$ q9 G. i" _) {; [, fImmunohistochemistry showed that the number
) I5 V# Y/ ?4 f5 J; |8 ?1 eof myenteric ICC was significantly higher/ A6 H; _3 t* X' a5 \9 R1 \8 H/ O5 K" J
in diabetic rats than that in the controls, and the( I" A: K- o5 M7 \3 _; P
expression of proximal colon ICC was decreased6 K% Z& B! L" H- |) y9 c6 E
with the time prolonging. Electron microscopy" u  @) X# a7 \' u5 M
exhibited damaged microstructures of colonic
, ?$ t7 g/ f" ^( p5 SICC such as swelling, vacuole-like degeneration
' E8 }* H+ Z$ k8 d5 w7 }of mitochondria and obvious decrease of
- c& `! f6 g$ Y0 T/ h7 morganelles. Meanwhile, the serum concentration, k4 J5 G" @+ ]' ^3 ]! U
of S-SCF was remarkably lower in diabetic rats
4 [, R; q5 g: l, sthan that in the controls (6 wk: 0.93 ± 0.53 μg/L3 m# ^  o3 u5 h3 P( S! s3 _
vs 1.87 ± 0.92 μg/L, P < 0.05; 8 wk: 0.78 ± 0.21 μg/L$ k; ~) G7 L" P" V% [- i2 g
vs 1.76 ± 0.94 μg/L, P < 0.05; 10 wk: 0.73 ± 0.20 μg/L- |% }. I/ V2 H8 X
vs 1.82 ± 0.96 μg/L, P < 0.05), but the content of
* ]$ P7 d' i/ u9 E. ]M-SCF in the colon tissues had no significant
( G* j4 y0 K) E# V3 O3 Wdifference between the diabetic and normal rats
6 p. p) `5 R% Q: Q, c. }) c, n(P > 0.05). The alteration trend of S-SCF concentration# |2 G. A9 b  F) N; t* p4 [2 N
was in accordance with that of ICC numbers.
; a: ~" d3 y4 L' iCONCLUSION: Decrease of colonic ICC quantity
; {! x$ e% [" V4 }and serum S-SCF concentration, and damaged
, y& _# E2 b8 y7 }microstructures of ICC are demonstrated in* P2 q: r; z" ]
diabetic rats with slow transit motility of colon,
, c, ~) G0 ~+ ^and these changes and their successive regulation
: B( }$ V  x6 R& E+ T- V' Q9 z' P2 c; gmay contribute to the pathogenesis of slow
8 I1 l' [2 v# S7 W+ G, u/ mtransit motility.
( V" O2 i% S3 q& f) a! a3 D2 SKey Words: Interstitial cells of Cajal; Stem cell factor;
( A, m' i/ j4 t% }% {" n- ZColon with slow transit motion; Diabetes mellitus+ Z2 a( B7 J9 U) M1 q: i
Luo Y, Lin L, Zhang HJ, Li XL, Wu GJ, Wang MF.+ {: a1 a" b, f) c' K4 I; m
Alteration of Cajal interstitial cells and stem cell factors in
' y$ f$ _& f- c' ?: W4 `colon with slow transit motility of diabetes mellitus. Shijie7 u4 d  o- M5 l
Huaren Xiaohua Zazhi 2007;15(5):458-463$ f/ [1 g" K, f( A
摘要
6 D6 O  ~! O  H3 ]目的: 了解Cajal间质细胞(ICC)、干细胞因子
7 f; N2 Q4 A* |; y. s(SCF)在糖尿病大鼠结肠慢传输运动模型中的
4 C2 j5 x$ j. x8 ?% [变化, 探讨其作用及可能的调控机制.
. {( z% F9 ]7 b1 f/ F$ ?! t方法: 54只♂SD大鼠分为糖尿病和正常对照
3 B* s! }$ [0 N+ g4 T9 m组, 经腹腔注射链脲佐菌素建立糖尿病大鼠2 v' e( Q( O, L, V1 k& X: Y+ o
模型, 于造模后6, 8, 10 wk各组分别处死9只大1 A% k" p; O) ~; P  p; `9 j; f+ F: h
鼠, 以免疫组化、透射电镜研究近端结肠组
( B7 ^4 d; D% O$ Q/ H1 k, r  b织中ICC的变化, 以Western blot方法检测近端+ ?2 x! W6 H9 F$ [/ b
结肠组织中膜结合型干细胞因子的表达, 以/ N: T( I" i9 ]+ z* a- ?
ELISA测定血清中可溶型SCF的浓度, 分析他
! u; T+ g! y6 I) \( `& D' W们之间的相关性./ p  i, R5 i3 l( l( T
结果: 糖尿病大鼠血糖随时间增加而升高, 而
* ?% Z5 h: Y: u8 ^胃肠推进率却降低(P >0.05). 免疫组化结果显
: c8 R# [' o; b. j8 H示, 6, 8, 10 wk时的糖尿病大鼠肌间ICC表达* R; W* p+ D* b1 i* z
较对照组明显减少(P <0.05), 且糖尿病大鼠近
; \! X$ D& @0 p端结肠ICC数量随时间推移有逐渐降少的趋3 K1 N& l9 L) k8 Z- i
势. 透射电镜显示糖尿病大鼠结肠ICC线粒体
" M2 p4 X) o0 R7 D+ m5 S肿胀、空泡样变, 细胞器数量明显减少. 与对
5 }* i; ]+ {) d! Q/ o8 q照组相比, 糖尿病大鼠血清中可溶型SCF显著/ K+ Z0 Q) Y6 T# U/ ~! G; m5 u$ b
降低(6 wk: 0.93±0.53 μg/L vs 1.87±0.92 μg/, I" F/ k) b; v3 y, S7 i( @
L, P <0.05; 8 wk: 0.78±0.21 μg/L vs 1.76±
) F; a/ W) c5 ?. b. X+ C3 Y) m0.94 μg/L, P <0.05; 10 wk: 0.73±0.20 μg/L vs6 D( ]7 B& [: p! g* }
1.82±0.96 μg/L, P <0.05), 而结肠组织中的膜
4 G! d8 ]. g+ h9 p结合型SCF无明显差异(P >0.05), 且可溶型干5 U+ ?% a) z% c7 o
细胞因子与ICC具有相同的变化趋势." A( ]! w% Z8 g* d9 v, A2 H0 W
结论: 糖尿病胃肠动力障碍大鼠存在血清中
4 {2 R  v8 V: P# J( s( B  x3 c2 `: a可溶性干细胞因子浓度下降以及结肠组织中7 \5 B* h$ J% P8 r) g
ICC数量减少和结构破坏, 这些变化及其可能4 T4 [0 V' d' ?6 f
存在的序贯性调控作用可能是糖尿病出现结
+ Z8 [( r( k- z; V1 F: }. H肠慢传输变化的基础.( j  z& F% |. c' h3 V9 `5 M
关键词: 干细胞因子; 糖尿病; 结肠慢传输运动;
# G) C( Y. n" J+ R+ X# }' A  cCajal间质细胞
# e8 s0 \& E( O6 p$ u1 d7 k: M罗云, 林琳, 张红杰, 李学良, 吴高珏, 王美峰. 糖尿病慢传输运
2 f: h* B  p+ \  P6 @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& p3 \- I! s8 }  m% F9 B' U* @/ L
2007;15(5):458-463  m) p# q) i5 I  k6 X6 ?

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