Catalpol prevents the loss of CA1 hippocampal neurons and reduces working errors in gerbils after ischemia-reperfusion injury

• Published in: Toxicon (Oxford) Vol. 46; no. 8; pp. 845 - 851
• Main Authors: Li, Dan-Qing, Li, Yang, Liu, Yuxin, Bao, Yong-Ming, Hu, Bo, An, Li-Jia
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 15.12.2005; Elsevier Science
• Subjects: Analysis of Variance; Animals; Behavioral Symptoms - drug therapy; Behavioral Symptoms - physiopathology; Biological and medical sciences; Catalpol; Cognition; Dose-Response Relationship, Drug; General pharmacology; Gerbillinae; Gerbils; Glucosides - chemistry; Glucosides - pharmacology; Glucosides - therapeutic use; Hippocampus; Hippocampus - cytology; Hippocampus - drug effects; Iridoid Glucosides; Iridoids - chemistry; Iridoids - pharmacology; Iridoids - therapeutic use; Ischemia; Medical sciences; Neurons - drug effects; Neuroprotection; Neuroprotective Agents - chemistry; Neuroprotective Agents - pharmacology; Neuroprotective Agents - therapeutic use; Pharmacognosy. Homeopathy. Health food; Pharmacology. Drug treatments; Reperfusion Injury - drug therapy; Reperfusion Injury - physiopathology; Time Factors; Neuroprotection; Gerbils; Cognition; Catalpol; Ischemia; Hippocampus; Central nervous system; Cardiovascular disease; Encephalon; Gesneriaceae; Prevention; Dicotyledones; Angiospermae; Root; Rodentia; Error; Neuroprotective agent; Biological activity; Vertebrata; Mammalia; Neuron; Animal; Plant origin; Spermatophyta; Gerbil
• ISSN: 0041-0101; 1879-3150
• DOI: 10.1016/j.toxicon.2004.09.007

Catalpol, an iridoid glycoside, contained richly in the roots of Rehmannia glutinosa, was found for the first time to be of neuroprotection in gerbils subjected to transient global cerebral ischemia. Catalpol (1 mg/kg ip) used immediately after reperfusion and repeatedly at 12, 24, 48 and 72 h significantly rescued neurons in hippocampal CA1 subfield and reduced working errors during behavioral testing. The neuroprotective efficacy of catalpol became more evident when the doses of catalpol were increased to 5 and 10 mg/kg. In addition, it was exciting that the significant neuroprotection by catalpol was also evident when catalpol was applied up to 3 h after ischemia. But the neuroprotective efficacy of catalpol became weak when catalpol was given at 6 h after ischemia. Of great encouragement was the finding that the neuroprotection of catalpol could be seen not only in a short post-ischemic period (12 days) but also in a long period (35 days). All these indicated that catalpol was truly neuroprotective rather than simply delayed the onset of neuronal damage and might be of therapeutic value for the treatment of global cerebral ischemia.