[Effects of puerarin on expression of nuclear factor kappaB after cerebral ischemia/reperfusion in rats].
Meiping Ding, Fei Feng, Haitao Hu
Abstract
Meiping Ding, Fei Feng, Haitao Hu
Abstract
OBJECTIVE: To investigate the activation of nuclear factor kappaB (NF-KB) and the influence of puerarin on it after cerebral ischemia-reperfusion in rats. METHOD: Cerebral ischemia-reperfusion injury was induced by 90 min of middle cerebral artery (MCA) occlusion and followed by 2, 6, 12, 24, 72 h reperfusion. Puerarin or saline was intra-peritoneally injected 1h before MCA occlusion and then the drugs were administered once every six hours. The infarct volume and brain edema were determined by TTC stain. Level of NF-kappaB P65 subunit was determined by immunohistochemistry and western blot. RESULT: Immunohistochemistry revealed the translocation of NF-kappaB. A time course of NF-kappaB induction in brain showed that NF-kappaB P65 subunit obviously increased at 6 h, peaked at 24 h and then decreased by 72 h post-reperfusion. Puerarin decreased the level of NF-kappaB at 24, 72 h after reperfusion. There was a decrease trend in brain infarct volume between puerarin and control. CONCLUSION: NF-kappaB is translocated and its level is increased after ischemia-reperfusion. Puerarin may attenuate the ischemia-reperfusion injury through inhibition of NF-kappaB activation.
OpenAlex reports 22 citations for this work. Citation counts describe recorded attention and do not establish research quality.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
OBJECTIVE: To investigate the activation of nuclear factor kappaB (NF-KB) and the influence of puerarin on it after cerebral ischemia-reperfusion in rats. METHOD: Cerebral ischemia-reperfusion injury was induced by 90 min of middle cerebral artery (MCA) occlusion and followed by 2, 6, 12, 24, 72 h reperfusion. Puerarin or saline was intra-peritoneally injected 1h before MCA occlusion and then the drugs were administered once every six hours. The infarct volume and brain edema were determined by TTC stain. Level of NF-kappaB P65 subunit was determined by immunohistochemistry and western blot. RESULT: Immunohistochemistry revealed the translocation of NF-kappaB. A time course of NF-kappaB induction in brain showed that NF-kappaB P65 subunit obviously increased at 6 h, peaked at 24 h and then decreased by 72 h post-reperfusion. Puerarin decreased the level of NF-kappaB at 24, 72 h after reperfusion. There was a decrease trend in brain infarct volume between puerarin and control. CONCLUSION: NF-kappaB is translocated and its level is increased after ischemia-reperfusion. Puerarin may attenuate the ischemia-reperfusion injury through inhibition of NF-kappaB activation.
Key concepts: Puerarin, Ischemia, Reperfusion injury, Western blot, Medicine, Immunohistochemistry, Pharmacology, Anesthesia