Panax Notoginseng Burk Attenuates Impairment of Learning and Memory Functions and Increases ED1, BDNF and β-Secretase Immunoreactive Cells in Chronic Stage Ischemia-Reperfusion Injured Rats

Abstract

Panax Notoginseng Burk (PN) has been reported to improve blood circulation, as well as learning and memory functions. The purpose of the present study was to investigate the effect of PN on learning and memory functions in chronic cerebral infarct rats. A cerebral infarct animal model was established by blocking the blood flow of both common carotid arteries and right middle cerebral artery for 90 min followed by reperfusion for 4 weeks. PN (0.5 g/kg) was administered orally 3 days per week for 4 weeks, whereas the control group provided bait and water only. The learning and memory functions were estimated by measuring how successful rats were able to negotiate an 8-arm radial maze test; the test was performed after operation once a week for 4 weeks. Finally, the rats were sacrificed and their brains were removed. The brains were sectioned and analyzed for ED1, glial fibrillary acid protein (GFAP), nuclear factor-kappaB, and brain derivative neurotrophin factor (BDNF) and beta-secretase by immunostaining. Cerebral infarct rats given PN were able to successfully navigate the 8-arm radial maze test four weeks after cerebral infarction. PN also increased ED1, BDNF and beta-secretase immunoreactive cells, but did not increase GFAP and NF-kappaB immunoreactive cells. PN attenuated the reduction in learning and memory functions induced by cerebral infarction in cerebral ischemia-reperfusion injured rats; it also increased the amount of activated microglia and BDNF. These data suggest that the effect of PN, at least in part, is closely related to the increase in BDNF that was generated by activated microglia. The effect that PN has on astrocytes, NF-kappaB and beta-secreatase immunoreactive cells requires further study.

Electro-acupuncture ameliorates cognitive impairment via improvement of brain-derived neurotropic factor-mediated hippocampal synaptic plasticity in cerebral ischemia-reperfusion injured rats

“…PSD-95 is a neuronal PDZ protein that associates with receptors and cytoskeletal elements at synapses (31). In the present study, the levels of PSD-95 were possibly regulated by BDNF, since certain studies reported the principal role of BDNF in synaptic plasticity and learning and memory processes (32)(33)(34). Inhibition of BDNF signaling has been previously shown to decrease hippocampal PSD-95 expression and dendritic growth (35).…”

Inhibition of Arterial Myogenic Responses by a Mixed Aqueous Extract of Salvia Miltiorrhiza and Panax Notoginseng (PASEL) Showing Antihypertensive Effects

“…Inhibition of voltage-operated Ca 2＋ channels or receptor-operated Ca 2＋ channels have previously been suggested as possible mechanisms of vasodilatation induced by Danshen and Sanchi (Sun et al, 2007;Chuang et al, 2008;Li et al, 2008). In the present study, therefore, we examined the effects of PASEL on high K ＋ -induced contraction and phenyleprine (PhE)-induced contraction of rat femoral arteries.…”

“…However, such studies were mostly performed with large conduit arteries that might not directly reflect the in vivo effects on microcirculation or on blood pressure. While not as popular as Danshen, Sanchi (三七根, Panax notoginseng) has also been used in treating circulatory disorders in TCM (Sun et al, 2007;Chuang et al, 2008;Li et al, 2008).…”

Ischemia signalling to Alzheimer-related genes

“…The production of β-amyloid peptide increases in the brain after ischemia, which impairs the memory [76]. Recent data have shown that ex perimental ischemic brain injury stimulates the expression, production and activity of Alzheimer's disease β-secretase in animal brain parenchyma [7,12,13,70]. Another study showed for the first time the alteration in mRNA expression of three amyloid precursor protein metabolism-related genes: β-secretase (BACE1), cathepsin B and glutaminyl cyclase mRNA, whose expression increased in the hippocampus and cortex quickly after ischemia-recirculation [78].…”