The effects of exercise preconditioning on cerebral blood flow change and endothelin-1 expression after cerebral ischemia in rats.

Stroke is an acute cerebrovascular disease with high incidence, morbidity, and mortality. Preischemic treadmill training has been shown to be effective in improving behavioral and neuropathologic indices after cerebral ischemia. However, the exact neuroprotective mechanism of preischemic treadmill training against ischemic injury has not been elucidated clearly. The present study investigated whether preischemic treadmill training could protect the brain from ischemic injury via regulating cerebral blood flow (CBF) and endothelin 1 (ET-1). We analyzed the CBF by laser speckle imaging and ET-1 expression by an enzyme-linked immunosorbent assay using an ischemic rat model with preischemic treadmill training. Generally speaking, ET-1 expression decreased and CBF increased significantly in the pretreadmill group. It is worth noting that ET-1 expression is increased at 24 hours of reperfusion in the pretreadmill group compared with the level of the time after middle cerebral artery occlusion. These changes were followed by significant changes in neurologic deficits and cerebral infarct volume. This study indicated that preconditioning exercise protected brain from ischemic injury through the improvement of CBF and regulation of ET-1 expression, which may be a novel component of the neuroprotective mechanism of preischemic treadmill training against brain injury.

The protective effect of curcumin against the 19­kDa Mycobacterium tuberculosis protein-induced inflammation and apoptosis in human macrophages.

The Mycobacterium tuberculosis 19-kDa lipoprotein (P19) is both cell wall-associated and secreted and is a candidate virulence factor that could cause the apoptosis of human macrophages infected with M. tuberculosis. P19 induces TLR2 activation, resulting in the upregulation of death receptors and ligands, followed by a death-receptor signaling cascade. The mechanisms by which P19 induces macrophage apoptosis are not fully characterized. Curcumin, a natural polyphenol, exhibits a variety of pharmacological effects such as antioxidant, anti-inflammatory and antitumor properties. In the present study, we investigated the effect of curcumin on P19-induced apoptosis in human macrophage cells and the underlying mechanisms. The results showed that both P19 and curcumin inhibit the growth of macrophages in a dose- and time-dependent manner. A low dose of curcumin (10 or 20 µM) attenuated both the macrophage cell growth inhibition and the increase in the expression of IL-6 and TNF-α induced by P19. Curcumin also decreased the phosphorylation of JNK and p38 that were induced by P19. However, JNK but not p38 inhibitors reversed the effect of P19 on the growth inhibition of macrophages. These data suggest that curcumin may protect macrophages from P19-induced cell apoptosis via a TLR2-mediated JNK-dependent pathway.

A case of tuberculous peritonitis.

This study aimed to provide the initial laparoscopy results as well as the results after a 16-month follow-up of a 78-year-old patient with tuberculous peritonitis. Imaging and laboratory examinations were performed for preliminary diagnosis, and laparoscopy and Gram staining were used for definitive diagnosis. The initial laparoscopy results showed the presence of typical yellow-white nodules on the liver surface and a biopsy demonstrated caseous necrotic granuloma. After 16 months, laparoscopy results showed that yellow-white nodules were reduced after antituberculous drug treatment and adhesions formed by fibrin networks were clearly visible. Laparoscopy and biopsy contributed to the rapid diagnosis of tuberculous peritonitis.