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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Cells, Cultured, Ginsenosides, Hippocampus, Neurons, Neuroprotective Agents, Nitric Oxide, Nitric Oxide Synthase, Radiation Injuries, Rats, Rats, Sprague-Dawley.
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Does [ Ginsenoside Rg1 protect rat hippocampal neurons from radiation injury by regulating NOS activity ]? Context: To study the protective effect of ginsenoside Rg1 on cultured rat hippocampal neurons against radiation injury and explore new therapies for preventing radiation encephalopathy. Rat hippocampal neurons cultured for 12 days were subjected to a single-dose X-ray exposure of 30 Gy. 4',6-diamidino-2-phenylindole (DAPI) staining was used to detect the neuronal apoptosis and NOS activity kit utilized to evaluate NOS activity in the cells after the exposure. Nuclear condensation was detected in (25.3-/+3.57)% of the neurons 24 h after 30 Gy X-ray exposure, a rate significantly higher than that in the control cells [(1.95-/+0.78)%, P<0.01]. In the neurons pretreated with ginsenoside Rg1, only (7.43-/+1.51)% of the cells presented with nuclear condensation after the exposure, significantly different from the rates in the control cultures and the exposed cultures (P<0.01). The NOS activity of exposed cultures was 6.46-/+0.95 U/ml, significantly higher than that in the control cultures (3.20-/+0.70 U/ml, P<0.01). The NOS activity of the neurons pretreated with ginsenoside Rg1 was 3.85-/+0.69 U/ml, significantly different from that in the control cultures (P<0.05) and the exposed cultures (P<0.01).
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Ginsenoside Rg1 offers significant protective effect on rat hippocampal neurons from radiation-induced apoptosis by reducing the activity of NOS. Final Decision: yes