|
- 积分
- 49
- 威望
- 49
- 包包
- 183
|
罗 云, 林 琳, 张红杰, 李学良, 吴高珏, 王美峰
7 J( n4 M" Q- }% w$ I: K( d- M罗云, 林琳, 张红杰, 李学良, 吴高珏, 王美峰, 南京医科大学5 V+ G9 v1 G: g0 I9 l* U
第一附属医院消化内科 江苏省南京市 2100294 Q) a* l: S0 b& y0 b) b$ W, K5 S6 l
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
' [" w( J) y# T- A: f& Z疾病.
) W+ W4 |5 u) W5 J江苏省“135工程”重点人才基金项目, No. RC2003087
. H2 e! |% ~% n. E% p" e0 Y' Y% M江苏省自然科学基金项目, No. BK2004158
h. ?6 n+ w" p通讯作者: 林琳, 210029, 江苏省南京市, 南京医科大学第一附
7 }5 O/ X8 N" A1 _属医院消化内科. lin9100@yahoo.com.cn
. k& {9 E" s2 ^' }# {2 Z/ r电话: 025-83781836-6920, I* M, d% w' L" p
收稿日期: 2006-11-29 接受日期: 2006-12-18+ [$ w) }% B1 D% H
Alteration of Cajal interstitial
/ s7 U% m, D* E( V( r; jcells and stem cell factors in
: _- X4 V6 V2 x/ @colon with slow transit motility; J6 v, I, X1 l" g; b
of diabetes mellitus; x: |, L7 k+ s# ~& @, e% v
Yun Luo, Lin Lin, Hong-Jie Zhang, Xue-Liang Li,/ p: L- K+ z! e, }7 c ?
Gao-Jue Wu, Mei-Feng Wang
! f$ |% t0 [1 mYun Luo, Lin Lin, Hong-Jie Zhang, Xue-Liang Li, Gao-8 L1 g4 x8 N9 {
Jue Wu, Mei-Feng Wang, Department of Gastroenterology,
9 n4 F1 P `# Rthe First Affiliated Hospital of Nanjing Medical University,
$ I; K0 D+ o8 j" }Nanjing 210029, Jiangsu Province, China: `4 o+ H' M8 N6 J7 }8 ]2 H) G0 }. L
Supported by the Natural Science Foundation of Jiangsu) H" w2 ?: g! w9 g( l3 h5 h
Province, No. BK2004158, and the Fund from “135 Project”
. B' I# r% X2 G& mfor the Key Talents of Health and Science Education2 j7 h* C2 y c, |3 N
Department of Jiangsu Province, No. RC2003087
& P6 i5 B" Y! bCorrespondence to: Lin Lin, Department of Gastroenterology,7 E9 f% e* ?2 V
the First Affiliated Hospital of Nanjing Medical4 u f* Q: L% e& c: v" V" Z3 T2 Z
University, Nanjing 210029, Jiangsu Province,
* V: A. y1 t/ t, h6 V4 p+ HChina. lin9100@yahoo.com.cn
. w. `3 U2 [0 V) H; a+ x GReceived: 2006-11-29 Accepted: 2006-12-18
' }( I# j$ B4 G$ S/ x7 \7 U/ ^( B% P9 BAbstract
9 a" a5 F ^% }8 O* A* tAIM: To observe the alterations of interstitial' y2 ~; D7 J! v. O# C
cells of Cajal (ICC) and stem cell factors (SCF)+ [3 r* l% B7 ]
in colon tissues with slow transit motility of
1 N" z0 \: j$ _! Idiabetes mellitus, and study their roles and
8 L6 p6 b/ M2 G/ apossible regulatory mechanism.3 y) C8 d7 J4 N8 S/ E8 }0 j
METHODS: A total of 54 male Sprague-Dawley% X! C k3 M" }% R% n8 p% v$ z8 w
rats were randomly and averagely divided into
2 L% A# l' f jdiabetes group and control group. Diabetes1 L9 c1 _0 R4 X& _5 J* Q) N; e
model was induced by intraperitoneal injection
' |0 `1 R5 u7 e& N, |4 Uof streptozotocin. Nine rats of the above8 D y! ^" ^) ~9 l- t, M
two groups were killed respectively 6, 8 and 10
& x0 B/ _6 L. Tweeks after injection. The alterations of ICC and5 [2 l, w. Y7 n! M, B
membrane-bound SCF (M-SCF) in the proximal
0 a6 i+ U4 N6 zcolon tissues were analyzed by immunohistochemistry,
# z; A2 l' O; X5 v6 qtransmission electron microscopy and8 p0 I. l( W' v g8 ?3 ]+ C. `
Western blot, and the serum concentration of8 U% s9 @8 S- M" f. Q9 G F
soluble SCF (S-SCF) were examined by enzymelinked
" q* @# N l/ B- a$ p" ^immunosorbent assay (ELISA).
8 |; D. ^2 v. n, n1 c% @# CRESULTS: The level of blood glucose was elevated
' J. `+ B2 y6 {5 j4 twhile the intestinal propulsive rate was
2 B. t+ ?3 H! x$ |lowered with the prolonging of time (P > 0.05).) W, C" f) O: z, L' L1 Z1 q( i2 ^
Immunohistochemistry showed that the number
1 c8 I! L) T) M8 V* X0 gof myenteric ICC was significantly higher
+ G* I1 n7 q9 Y7 d" Q4 m. }in diabetic rats than that in the controls, and the# g: g8 r/ ~$ M! }$ R
expression of proximal colon ICC was decreased
7 r2 Z& ^8 {6 n |# Swith the time prolonging. Electron microscopy
$ x% t* M. g5 }' ]- K6 j5 }" V( mexhibited damaged microstructures of colonic) d7 F. L! m% ?6 q- _6 [/ W
ICC such as swelling, vacuole-like degeneration
/ N* ?, H' [$ g6 b6 cof mitochondria and obvious decrease of
4 _+ Q& ]! j: J1 K) u7 G4 xorganelles. Meanwhile, the serum concentration
( }; V* B6 \9 B+ g [of S-SCF was remarkably lower in diabetic rats
# s3 J9 W! F/ o9 c1 Y3 s( V0 x3 ]than that in the controls (6 wk: 0.93 ± 0.53 μg/L/ l2 R' q6 F+ s; g* n$ y0 U
vs 1.87 ± 0.92 μg/L, P < 0.05; 8 wk: 0.78 ± 0.21 μg/L
3 \( Y* ^9 }$ { cvs 1.76 ± 0.94 μg/L, P < 0.05; 10 wk: 0.73 ± 0.20 μg/L
; J1 t" A" g2 A- m3 Y7 vvs 1.82 ± 0.96 μg/L, P < 0.05), but the content of
- T6 ? V, `7 W8 m3 V$ rM-SCF in the colon tissues had no significant3 j( @8 e; Q8 K( V( C0 s* ?- Q
difference between the diabetic and normal rats+ }- y2 z! {6 W1 U3 X) C q
(P > 0.05). The alteration trend of S-SCF concentration0 \& K) V7 P) c1 i" m3 z
was in accordance with that of ICC numbers.1 O2 K2 j2 x4 ^$ o( Y" ?3 o+ _+ N6 I
CONCLUSION: Decrease of colonic ICC quantity
6 U0 B* m" D# d5 q5 \and serum S-SCF concentration, and damaged
1 D; K* R$ E7 C4 v9 G$ _6 imicrostructures of ICC are demonstrated in0 z5 G6 W( i3 |# n) m
diabetic rats with slow transit motility of colon,: @0 I3 I' x# Z. K& X/ m% O8 I. @
and these changes and their successive regulation0 E2 y7 \' l5 S
may contribute to the pathogenesis of slow- {$ ^ P, y& J
transit motility.
4 C% c) c: }. {) z1 R; J5 MKey Words: Interstitial cells of Cajal; Stem cell factor;6 M- P1 ]3 ^- C( Y- a4 m3 y
Colon with slow transit motion; Diabetes mellitus% d$ \8 V! y9 Z9 Y% N
Luo Y, Lin L, Zhang HJ, Li XL, Wu GJ, Wang MF.2 X9 a- L# M& ~7 m
Alteration of Cajal interstitial cells and stem cell factors in' K4 S) d7 U3 ^8 M
colon with slow transit motility of diabetes mellitus. Shijie7 P5 L: v$ T# ^5 ~. o
Huaren Xiaohua Zazhi 2007;15(5):458-463
, x" ^) Q5 u+ y' k摘要. E1 Z! T$ q/ N8 n& T
目的: 了解Cajal间质细胞(ICC)、干细胞因子
8 z; s: s W% x+ l; s(SCF)在糖尿病大鼠结肠慢传输运动模型中的/ f) L, o1 z3 ]' `1 _
变化, 探讨其作用及可能的调控机制.% `( r0 d: @. g3 p& w
方法: 54只♂SD大鼠分为糖尿病和正常对照
7 w& e5 c: E9 v2 D4 z! n组, 经腹腔注射链脲佐菌素建立糖尿病大鼠+ B* t4 s4 s3 ?8 P- V3 J
模型, 于造模后6, 8, 10 wk各组分别处死9只大% Z+ i4 ~$ U+ l8 @, W- D
鼠, 以免疫组化、透射电镜研究近端结肠组3 F$ e# w1 R" p
织中ICC的变化, 以Western blot方法检测近端
/ D) U0 o7 Z+ V5 P结肠组织中膜结合型干细胞因子的表达, 以: Z* A# C; v9 T W
ELISA测定血清中可溶型SCF的浓度, 分析他! w" d+ f. p* `0 T
们之间的相关性.+ M4 d/ \* m' o) Y9 l* P
结果: 糖尿病大鼠血糖随时间增加而升高, 而
9 D0 s$ F l' o7 V胃肠推进率却降低(P >0.05). 免疫组化结果显
- N# c6 P( ~3 p. C+ s( ~: F示, 6, 8, 10 wk时的糖尿病大鼠肌间ICC表达
2 E. v4 K1 q5 y% S较对照组明显减少(P <0.05), 且糖尿病大鼠近" N1 p) V0 j( j! M* C1 _. T/ A: X
端结肠ICC数量随时间推移有逐渐降少的趋8 B1 X- O! ~$ n! d3 t- t& ?) y
势. 透射电镜显示糖尿病大鼠结肠ICC线粒体
* Q5 [# ]+ \4 l \, y( s( {肿胀、空泡样变, 细胞器数量明显减少. 与对
) l' W2 ^" g5 l照组相比, 糖尿病大鼠血清中可溶型SCF显著
% ?3 [+ ^- ]' m9 E降低(6 wk: 0.93±0.53 μg/L vs 1.87±0.92 μg/. J3 Z5 T" H) X- l2 H
L, P <0.05; 8 wk: 0.78±0.21 μg/L vs 1.76±* E7 O' Y$ R* R; ?/ j8 m, h: W
0.94 μg/L, P <0.05; 10 wk: 0.73±0.20 μg/L vs4 L) F) P# r7 @6 z
1.82±0.96 μg/L, P <0.05), 而结肠组织中的膜2 t9 d# A; K: {2 f$ Z9 I
结合型SCF无明显差异(P >0.05), 且可溶型干
2 k" n* O; K- \细胞因子与ICC具有相同的变化趋势./ j4 b. F5 {4 [% i
结论: 糖尿病胃肠动力障碍大鼠存在血清中
7 ]! B, W8 v4 @: U5 b6 F可溶性干细胞因子浓度下降以及结肠组织中
; K* r$ x7 k8 M* \1 ^$ mICC数量减少和结构破坏, 这些变化及其可能
( G; D. H4 b; @4 o$ Y存在的序贯性调控作用可能是糖尿病出现结, _( v0 V! d( Z/ p7 n
肠慢传输变化的基础.* d% g7 V, u- l: S* ]8 L
关键词: 干细胞因子; 糖尿病; 结肠慢传输运动;
" X: w2 P6 Q8 h6 h' j, uCajal间质细胞% T/ p- a* p9 `6 S
罗云, 林琳, 张红杰, 李学良, 吴高珏, 王美峰. 糖尿病慢传输运& q+ N d& H4 c9 p; l8 }$ c
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 C* M/ a0 G6 l1 ^! z( v; t' y- u
2007;15(5):458-463
3 H! P* t& ` Y+ ^
t2 u( m6 `6 D附件是pdf全文。感谢大家支持，回复本贴就可以下载了) @% S4 T+ l3 s0 y" C5 Z
6 d7 d( K2 i; L6 y[hide][/hide] |
附件: 你需要登录才可以下载或查看附件。没有帐号？注册
|
发表于 2009-3-2 11:23
