Effects of hypothalamic paraventricular nuclei on apoptosis and proliferation of gastric mucosal cells induced by ischemia/reperfusion in rats

Figure 1 Sites of the stimulating electrode tip in PVN. A: Standard atlas sections of the rat brain showing the distributions of stimulating sites of the experimental animals; B: Photomicrographs of stimulating sites in the rat brain. The section stained with neutral red, showing the position of stimulating electrode tip by passing a positive DC of 1 mA for 10 s, which indicates a placement within the PVN.

Figure 2 Effect of electrical stimulation and bilateral electrolytic destruction of PVN on gastric mucosal damage induced by I/R at 1 h after reperfusion in rats. Intact: normal rat; sham: sham-operation (electrode was inserted, with no current passing and no artery clamped); ES + N: intact stomach after electrical stimulation of the PVN. EL + N: intact stomach after bilateral electrolytic destruction of the PVN; GI/R injury: gastric ischemia-reperfusion injury; Sham+GI/R injury: sham electrical stimulation of the PVN plus GI/R injury; ES: electrical stimulation of the PVN plus GI/R injury; EL: bilateral electrolytic destruction of the PVN plus GI/R injury. Values of GMDI are mean ± SE (n = 6). ^bP < 0.01 vs intact, ^dP < 0.01 ES vs ES + N, ^fP < 0.01 EL vs EL + N, ^aP < 0.05, ES vs GI-R, ^cP < 0.05, EL vs ES.

Figure 3 Effect of electrical stimulation of PVN on gastric mucosal damage induced by I/R at different times in rats. Sham: sham-operation(electrode was inserted, with no current passing and no artery clamped); GI/R: gastric ischemia/reperfusion was maintained for 30 min, 1 h, 3 h and 6 h after 30 min of ischemia, respectively; PVN + GI/R: electrical stimulation of the PVN plus GI/R. Values: Each column represents mean ± SE (n = 6). ^bP < 0.01 vs sham; ^aP < 0.05, ^dP < 0.01, PVN + GI/R vs GI/R at different times.

Figure 4 Histological exhibition of electrical stimulation of PVN on gastric mucosal apoptosis induced by I/R at different times in rats. The apoptotic-positive cells were probed with anti-M30 CytoDEATH antibody and counter-stained with hematoxylin in rat gastric mucosa (× 400). A: normal gastric mucosa; B: sham operation; C: GI/R at 1 h after reperfusion; D: PVN + GI/R at 1 h after reperfusion; E: GI/R at 6 h after reperfusion; F: PVN+GI/R at 6 h after reperfusion; G: negative control group.

Figure 5 Effect of electrical stimulation of PVN on gastric mucosal cellular apoptosis induced by I/R at different time points in rats. Sham: sham-operation; GI/R: reperfusion was maintained for 30 min, 1 h, 3 h and 6 h after 30 min of ischemia, respectively; PVN + GI/R: electrical stimulation of PVN plus GI/R. The percentage of apoptotic cells was taken by counting the cells in 10 microscopic fields (× 400). Each column represents mean ± SE (n = 6). ^aP < 0.05, ^bP < 0.01, GI/R vs sham-operation; ^cP < 0.05, ^dP < 0.01, PVN + GI/R vs GI/R at each time point.

Figure 6 Histological exhibition of electrical stimulation of PVN on gastric mucosal cellular proliferation induced by I/R at different times in rats. Proliferating-positive cells were probed with anti-mouse anti-proliferating cell nuclear antigen (PCNA) antibody and counter stained with hematoxylin in gastric mucosa (× 100). A: normal control gastric mucosa; B: gastric mucosa after sham operation; C: GI/R, 1 h after reperfusion; D: PVN + GI/R, 1 h after reperfusion; E: GI/R, 6 h after reperfusion; F: PVN + GI-R, 6 h after reperfusion; G: negative control group.

Figure 7 Effect of electrical stimulation of PVN on gastric mucosal proliferation induced by I/R at different times in rats. Sham: sham-operation; GI/R: reperfusion was maintained for 30 min, 1 h, 3 h and 6 h after 30 min of ischemia, respectively; PVN+GI/R: electrical stimulation of PVN plus GI/R. The percentage of proliferating cells was taken by using cell count in 10 microscopic fields (× 100). Each column represents an average value expressed in mean ± SE (n = 6). ^bP < 0.01, GI/R vs sham operation; ^aP < 0.05 and ^dP < 0.01, PVN + GI/R vs GI/R.