Effects of p38 Mitogen-Activated Protein Kinase on Apoptosis of Small Intestinal Epithelial Cells after Transplantation in Rats_CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Authors：

ZHANG Jian , HU Xiang.

Department of General Surgery, The First Affiliated Hospital, Dalian Medical University, Dalian 116011, China;

Corresponding author：

Keywords：

Small intestinal transplantation Rejection reaction Cell apoptosis Tumor necrosis factor-α p38 mitogen-activated protein kinase

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【Abstract】ObjectiveTo explore the effects of p38 mitogenactivated protein kinase (MAPK) on apoptosis of small intestinal epithelial cells after transplantation in rats.
MethodsSmall intestinal transplantation was performed in SD and Wistar rats. The recipients were divided into three groups: isograft group (Wistar→Wistar group), allograft group (SD→Wistar group) and allograft+cyclosporine A group (SD→Wistar+CsA group). The grafts were harvested on day 1, 3, 5 and 7 after operation. All graft samples were subjected to histological examination. The apoptosis of graft epithelial cells was detected by TUNEL method. p38 MAPK was measured by Westernblotting method and serum TNFα was determined by ELISA.
ResultsMild, moderate and severe rejection reaction occurred in the SD→Wistar group, it was showed that the number of apoptotic cells increased with the severity of the rejection reaction by TUNEL. In SD→Wistar group, the numbers of apoptotic cells were significantly higher than those of the other two groups （P＜0.01）. The severity of rejection reaction in SD→Wistar+CsA group was less than that of SD→Wistar group and the number of apoptotic cells increased with the severity of the rejection reaction (P＜0.01). The level of serum TNFα varied with the apoptotic degree of small intestinal epithelial cells in SD→Wistar group and SD→Wistar+CsA group （P＜0.01）. The expression of p38 MAPK increased with the number of the apoptotic cells in SD→Wistar group and SD→Wistar+CsA group （P＜0.01）, but there was no evident change in Wistar→Wistar group （P gt;0.05）. The expression of p38 MAPK and the level of serum TNFα were positively correlated with apoptosis in small intestinal rejection after transplantation （r=0.875， P＜0.01； r=0.837， P＜0.01）. p38 MAPK and TNFα were also positively correlated （r=0.826，P＜0.01）.
ConclusionApoptosis plays an important role in small intestinal rejection. p38 MAPK is involved in apoptosis and is an important regulator in signal pathway of cell apoptosis.

Citation： ZHANG Jian,HU Xiang.. Effects of p38 Mitogen-Activated Protein Kinase on Apoptosis of Small Intestinal Epithelial Cells after Transplantation in Rats. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 2006, 13(1): 66-70. doi: Copy

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10.	Cerwenka A, Kovar H, Majdic O, et al. Fas and activationinduced apoptosis are reduced in human T cells preactivated in the presence of TGFbeta 1 [Ｊ]. J Immunol, 1996; 156(2)∶459.
11.	Wei S, Liu JH, EplingBurnette PK, et al. Critical role of Lyn kinase in inhibition of neutrophil apoptosis by granulocytemacrophage colonystimulating factor [Ｊ]. J Immunol, 1996; 157(11)∶5155.
12.	Han J, Lee JD, Bibbs L, et al. A MAP kinase targeted by endotoxin and hyperosmolarity in mammalian cells [Ｊ]. Science, 1994; 265(5173)∶808.
13.	姜勇，刘爱华，张琳，等. 脂多糖激活p38在诱导肿瘤坏死因子α基因表达中的作用 [Ｊ]. 中华医学杂志， 1999； 79（5）∶360.

1. Lee RG, Tsamandas AC, AbuElmagd K, et al. Histologic spectrum of acute cellular rejection in human intestinal allografts [Ｊ]. Transplant Proc, 1996; 28(5)∶ 2767.
2. Krams SM, Hayashi M, Fox CK, et al. CD8+ cells are not necessary for allograft rejection or the induction of apoptosis in an experimental model of small intestinal transplantation [Ｊ]. J Immunol, 1998; 160(8)∶3673.
3. Schmid T, Oberhuber G, Korozsi G, et al. Histologic pattern of small bowel allograft rejection in the rat. Mucosal biopsies do not provide sufficient information [Ｊ]. Gastroenterology, 1989; 96(6)∶1529.
4. Rosemurgy AS, Schraut WH. Small bowel allografts. Sequence of histologic changes in acute and chronic rejection [Ｊ]. Am J Surg, 1986; 151(4)∶470.
5. Lomo J, Blomhoff HK, Beiske K, et al. TGFbeta 1 and cyclic AMP promote apoptosis in resting human B lymphocytes [Ｊ]. J Immunol, 1995; 154(4)∶1634.
6. Smyth MJ, Trapani JA. Granzymes: exogenous proteinases that induce target cell apoptosis [Ｊ]. Immunol Today, 1995; 16(4)∶202.
7. Kerr JF, Winterford CM, Harmon BV. Apoptosis. Its significance in cancer and therapy [Ｊ]. Cancer, 1994； 73(8)∶2013.
8. Ogawa N, Dang H, Talal N. Apoptosis and autoimmunity [Ｊ]. J Autoimmun, 1995; 8(1)∶1.
9. Raff MC, Barres BA, Burne JF, et al. Programmed cell death and the control of cell survival: lessons from the nervous system [Ｊ]. Science, 1993; 262(5134)∶695.
10. Cerwenka A, Kovar H, Majdic O, et al. Fas and activationinduced apoptosis are reduced in human T cells preactivated in the presence of TGFbeta 1 [Ｊ]. J Immunol, 1996; 156(2)∶459.
11. Wei S, Liu JH, EplingBurnette PK, et al. Critical role of Lyn kinase in inhibition of neutrophil apoptosis by granulocytemacrophage colonystimulating factor [Ｊ]. J Immunol, 1996; 157(11)∶5155.
12. Han J, Lee JD, Bibbs L, et al. A MAP kinase targeted by endotoxin and hyperosmolarity in mammalian cells [Ｊ]. Science, 1994; 265(5173)∶808.
13. 姜勇，刘爱华，张琳，等. 脂多糖激活p38在诱导肿瘤坏死因子α基因表达中的作用 [Ｊ]. 中华医学杂志， 1999； 79（5）∶360.

CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Effects of p38 Mitogen-Activated Protein Kinase on Apoptosis of Small Intestinal Epithelial Cells after Transplantation in Rats

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