Background and aims-Injuries caused by ischaemia and ischaemia/reperfusion in the small intestine have been widely accepted as resulting in necrosis. The aim of this study was to ascertain whether apoptosis also occurs. Methods-Intestinal epithelium from rats subjected to ischaemia (15-90 minutes) and ischaemia/reperfusion (15 minutes ischaemia followed by 15-75 minutes of reperfusion) was studied using histological, immunohistochemical, and molecular biological methods as well as FACS. Results-Mucosal injury was induced by both ischaemia and ischaemia/reperfusion. Detachment of epithelial cells from the villous stroma was an early morphological change indicating mucosal injury. More than 80% of the detached cells exhibited characteristic morphological features of apoptosis (condensation of chromatin and nuclear fragmentation).The remainder demonstrated necrotic features. The apoptotic cells eventually underwent spontaneous degeneration with membrane rupture, a process morphologically identical to necrosis. DNA fragmentation was also confirmed by immunohistochemical methods and agarose gel electrophoresis. Conclusion-Apoptosis is a major mode of cell death in the destruction of rat small intestinal epithelial cells induced by ischaemia and ischaemia/reperfusion injury. Disruption of epithelial cell-matrix interactions ("anoikis") may play an important part in induction of apoptosis in detached enterocytes. (Gut 1998;42:530-537)

Hunting for an effective medicine for brain stroke has been a medical task in neuroscience for decades. The present research showed that the lyophilized Powder of Catalpol and Puerarin (C-P) in all the tested doses (65.4 mg/kg, 32.7 mg/kg, 16.4 mg/kg) significantly reduced the neurological deficiency, infarct volume and apoptotic cells in ischemic/reperfusion (I/R) rats. It also promoted astrocyte processes and prolonged neuron axons in infarct area. Further, it decreased MDA, NO, NF-κB/p65, TNF-α, IL-1β and IL-6 and enhanced the EPOR and GAF-43. 65.4 mg/kg and 32.7 mg/kg C-P could up-regulated EPO and VEGF significantly. In vitro, 49 μg/mL and 24.5 μg/mL C-P decreased the leakage of sodium fluorescein and increased the activity of γ-GTP. Additionally, it increased SOD and decreased MDA, NO, and LDH and decreased NF-κB/p65, TNF-α, IL-1β and IL-6 and unregulated EPO, EPOR, VEGF, and GAP-43. Only the dose of 49 μg/mL increased TEER and Claudin-5 and turned the typically damaged morphologies of neurons, astrocytes and endothelium into a favorable trend. These data imply that C-P improved the recovery of neurological deficiency in motor, sense, balance and reflex, and protected the whole NVU by anti-oxidative stress, anti-inflammation and up-regulating some protective factors. This research provides a candidate medicine for brain stroke and, at the same time, a pattern for drug study targeting NVU in vitro.

Stroke is a serious disease with complex pathomechanism and limited therapeutic effect in clinic. Our previous research has found obvious therapeutic effect of Puerarin (Pur) on stroke injury of rat. The aim of this study is to investigate the transcriptome changes of oxygen-glucose deprivation/reoxygenation (OGD/R)-injured astrocytes before and after the intervention of Pur. Cells activity and apoptosis detection indicated that the activity of OGD/R-injured astrocytes was improved, and the apoptosis was ameliorated by Pur. Affymetrix GeneChip Rat Genome 230 2.0 Array assays indicated that after intervention of Pur, mRNA expressions of 31 genes were up-regulated and 40 genes were down-regulated in OGD group, whereas mRNA expression of 36 genes were up-regulated, and 88 genes were down-regulated in OGD/R group. Pathway analysis indicated that the olfactory transduction pathway and the JAK (janus kinase) 2/STAT (signal transducer and activator of transcription) three pathways were down-regulated by Pur during OGD/R injury of astrocytes. These data indicated that Pur regulates transcriptome and expresses protective effect on astrocytes during OGD/R injury, and may be a potential therapeutic agent for the treatment of stroke.

Repair of superficial damage to gastrointestinal mucosa occurs by a process called restitution. Goblet cells reside throughout the length of the intestine and are responsible for the production of mucus. However, a kinetic analysis of goblet cell dynamics of small intestine in restitution has hitherto not been reported. The aim of the present study was to investigate the role of goblet cells in the process of restitution of rat small intestine subjected to ischemia and ischemia-reperfusion injury, and therefore intestinal epithelium from rats subjected to both ischemia and ischemia-reperfusion was studied. Detachment of enterocytes was observed after 5-min of reperfusion. After 20-30 minutes of reperfusion, the denuded villous tips were covered with goblet cells. Within 75 min of reperfusion the epithelium restitution was complete. On the other hand, restitution was not observed in ischemia group. These data suggest that goblet cells may play an important role in restitution after ischemia-reperfusion injury.

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