ABSTRACT
AIM To investigate if the protective effect of baicalin on cerebral injury induced by transient focal ischemia is related to modulation of expressions of inflammatory cytokines or adhesive molecules. METHODS Transient focal cerebral ischemia injury model in rats was induced by occlusion of the right middle cerebral artery for 2 h, followed by 24 h reperfusion. The infarct volume and neurological deficit were determined by TTC staining and the scoring method of Longa et al. The expression of intracellular adhesion molecule-1 (ICAM-1), neutrophils infiltration, and myeloperoxidase (MPO) activity in brain were measured by immunohistochemistry, hematoxylin-eosin staining, and spectrophotometer, respectively. Semiquantitative RT-PCR was employed to assess the expression of inducible nitric oxide synthase (iNOS) mRNA. The level of interleukin-1 (IL-1) in brain was assayed by radioimmunoassay. The expression of nuclear factor-κB (NF-κB) protein was evaluated by Western blot. RESULTS After transient cerebral ischemia, MPO activity and the expression of ICAM-1 in the periphery of ischemic cortex were significantly increased. Increase in iNOS mRNA and NF-κB protein expression was also shown in the ischemic area. Treatment with baicalin markedly reduced brain infarct volume and neurological deficit induced by ischemic insult, inhibited MPO activity, inflammatory cell infiltration, as well as expression of ICAM-1, iNOS and NF-κB, and decreased IL-1 level. CONCLUSION Baicalin may play a protective effect on cerebral ischemic injury through inhibiting the expression and release of the inflammatory mediators after cerebral ischemia.
ABSTRACT
AIM: To study the protective effects of baicalin on myocardial ischemia-reperfusion injury in rats. METHODS: The models of myocardial ischemia-reperfusion injury were established by occluding left anterior descending coronary artery (LAD) for 30 min, followed by reperfusion for 120 min. The rate of rise and decline of left ventricular pressure (±dp/dtmax) and end-diastolic pressure of left ventricle (LVEDP) were monitored continuously with polygraph. After reperfusion, the blood and myocardium samples were taken for determination of malondialdehyde (MDA) content, superoxide dismutase (SOD), Na+-K+-ATPase, Ca2+-ATPase activities in myocardium, creatine kinase (CK) and lactate dehydrogenase (LDH) in serum with spectrophotometer. The ultrastructural changes in ischemic myocardium were assessed by transmission electron microscope. RESULTS:dtmax and LVEDP, decreased plasma CK and LDH levels, reduced myocardial MDA content, and increased the activities of SOD, Na+-K+-ATPase, and Ca2+-ATPase in myocardium following ischemia-reperfusion. The ultrastructural injury in reperfused myocardium was relieved. CONCLUSION: Baicalin possesses a protective effect against myocardial ischnemia-reperfusion injury through scavenging oxide radicals and improving Na+-K+-ATPase and Ca2+-ATPase activities.
ABSTRACT
Aim To investigate the protective effect of rosiglitazone on cerebral ischemia/reperfusion injury inrats. Methods Transient focal cerebral ischemia injury model in rats was induced by occlusion of the right middle cerebral artery for 2 h, followed by 24 h reperfusion. The infarct volume and neurological deficit were determined by the method of TTC staining and the Longa′s score, and used to evaluate the effect of rosiglitazone on cerebral injury. The levels of malondialdehyde (MDA), nitric oxide (NO), activities of superoxide dismutase (SOD), myeloperoxidase (MPO) and nitric oxide synthase (NOS) in brain were measured by spectrophotometer. Immunohistochemistry was employed to assess the expression of intracellular adhesion molucule-1 (ICAM-1). The histopathological change was observed after HE staining. Results Pretreatment with rosiglitazone markedly reduced brain infarct volume and neurological deficit induced by transient ischemia, inhibited MPO activity, as well as expression of ICAM-1; it also decreased NO, MDA levels and NOS activity, increased SOD activity, and improved histopathological injury. Conclusion Rosiglitazone has a protective effect on cerebral ischemia/reperfusion injury through inhibiting inflammatory process and lipid peroxidation.