Basic Research
Copyright ©The Author(s) 2003.
World J Gastroenterol. May 15, 2003; 9(5): 1028-1033
Published online May 15, 2003. doi: 10.3748/wjg.v9.i5.1028
Figure 1
Figure 1 Effect of EA on mC/mB. aP < 0.05, bP < 0.01 vs normal control; dP < 0.01, fP > 0.05 vs UC control; eP < 0.05 vs UC+EA at non-acupoint.
Figure 2
Figure 2 Colonic ultrastructure of UC control group: A, goblet cells, microvilli, endoplasmic reticula and mitochondria (TEM × 10000); B, inflammatory cells (TEM × 2500).
Figure 3
Figure 3 Colonic ultrastructure of UC+EA at ST36 group: A, goblet cells (TEM × 4000); B microvilli and mitochondria (TEM × 8000).
Figure 4
Figure 4 Colonic ultrastructure of EA+non-acupoint group: A, goblet cells, microvilli and mitochondria (TEM × 8000); B, endoplasmic reticula and mitochondria (TEM × 10000).
Figure 5
Figure 5 Effect of EA on colonic MPO activity. bP < 0.01 vs normal control; cP < 0.05, fP > 0.05 vs UC control; eP < 0.05 vs UC+EA at non-acupoint.
Figure 6
Figure 6 Effect of EA on TNF-α mRNA expression. A: Repre-sentative pictures of RT-PCR. Lane 1, 4, 7, 9: β-actin. Lane 2, 3, 6, 8: TNF-α. Lane 5, 10: DNA Marker (DL2000). B: Relative level of TNF-α mRNA expression. bP < 0.01 vs normal control; dP < 0.01, fP > 0.05 vs UC control; gP < 0.01 vs UC+EA at non-acupoint.
Figure 7
Figure 7 Effect of EA on serum TNF-α concentration. bP < 0.01 vs normal control; dP < 0.01, fP > 0.05 vs UC control; eP < 0.05 vs UC+EA at non-acupoint.