ETHNOPHARMACOLOGICAL RELEVANCE: Tongluojiunao (TLJN) is an herb extract that mainly contains ginsenoside Rg1 and geniposide, which are clinically used for treating ischemic damages in the brain. AIM OF THE STUDY: In the stroke, cerebral ischemia followed by oxygen reperfusion induced apoptosis in hippocampal neurons, while extension of axons and dendrites in neurons may compensate for and repair damages of neuronal network in the hypoxia brain. In this study, we investigated whether TLJN can protect neurons against damages by ischemia in brain vasculature. MATERIALS AND METHODS: We measured cell viability and lactate dehydrogenase (LDH) release from primary culture of rat hippocampal neurons before and after the neurons were deprived of oxygen and glucose (OGD). In addition, the effects were evaluated with cell viability and neurite outgrowth before or after OGD. RESULTS: We found that TLJN could play a neuroprotective role to cultured primary rat hippocampal neurons under both normal and oxygen/glucose-deprivation (OGD) conditions. TLJN could protect both cultured primary rat hippocampal neurons and brain microvascular endothelial cells (BMECs) from cell death under both normal and oxygen/glucose-deprivation (OGD) conditions. Moreover, under the same conditions, BMECs-conditioned media pretreated by TNJN could also promote neuron viability and neurite outgrowth, indicating that TLJN stimulated BMECs to secret some neuroprotective/neurotrophic factors. CONCLUSION: These findings suggest that TLJN has a marked neuroprotective and neurotrophic roles by either direct or indirect operation, and provide insight into the mechanism of clinical efficacy of this drug against stroke.
ETHNOPHARMACOLOGICAL RELEVANCE: Tongluojiunao (TLJN) is an herb extract that mainly contains ginsenoside Rg1 and geniposide, which are clinically used for treating ischemic damages in the brain. AIM OF THE STUDY: In the stroke, cerebral ischemia followed by oxygen reperfusion induced apoptosis in hippocampal neurons, while extension of axons and dendrites in neurons may compensate for and repair damages of neuronal network in the hypoxia brain. In this study, we investigated whether TLJN can protect neurons against damages by ischemia in brain vasculature. MATERIALS AND METHODS: We measured cell viability and lactate dehydrogenase (LDH) release from primary culture of rat hippocampal neurons before and after the neurons were deprived of oxygen and glucose (OGD). In addition, the effects were evaluated with cell viability and neurite outgrowth before or after OGD. RESULTS: We found that TLJN could play a neuroprotective role to cultured primary rat hippocampal neurons under both normal and oxygen/glucose-deprivation (OGD) conditions. TLJN could protect both cultured primary rat hippocampal neurons and brain microvascular endothelial cells (BMECs) from cell death under both normal and oxygen/glucose-deprivation (OGD) conditions. Moreover, under the same conditions, BMECs-conditioned media pretreated by TNJN could also promote neuron viability and neurite outgrowth, indicating that TLJN stimulated BMECs to secret some neuroprotective/neurotrophic factors. CONCLUSION: These findings suggest that TLJN has a marked neuroprotective and neurotrophic roles by either direct or indirect operation, and provide insight into the mechanism of clinical efficacy of this drug against stroke.