The pharmacological properties of magnolol and hOnokiol, neolignane derivatives, extracted from Magnolia officinalis, used in Chinese and Japanese traditional medicine, for neurosis and gastrointestinal complaints, were investigated. Magnolol and hOnokiol produced sedation, ataxia, muscle relaxation and a loss of the righting reflex with an increase in dose of 50 to 500 mg/kg i.p. Magnolol and hOnokiol at a dose of 50 mg/kg suppressed spinal reflexes in young chicks in a similar manner, but with a much longer duration of action than mephenesin. Pretreatment of mice with magnolol 100 mg/kg inhibited tonic extensor convulsions and death produced by an intracerebroventricular injection of penicillin 0 potassium 50 tg. In rats, after an intraventricular injection of penicillin G 400 .tg. magnolol suppressed the incidence of spike discharge, but not seizure discharge. Magnolol produced spindle discharges in sensory and motor cortex electroencephalograms and inhibited mid brain reticular formation-and hypothalamus-stimulated responses in the neo-and palaeo-cortex electroencephalograms, respectively. These results suggest that magnolol causes a depression of the ascending activating systems as well as of the spinal cord.

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Aim: We aimed to investigate whether the agonists for liver X receptor (LXR) ameliorate lupus-like phenotypes in mice mediated by the clearance of apoptotic cells, and compare with peroxisome proliferator-activated receptor (PPAR) γ plus PPARδ agonists, which also facilitate the clearance of apoptotic cells and exert anti-inflammatory effects in systemic lupus erythematosus (SLE). Methods: We investigated the efficacy of LXR agonist (GW3965) or dual treatment of PPARγ (pioglitazone) and PPARδ (GW0742) agonists in SLE animal models, female MRL/MpJ-Fas/J mice and BALB/cAJcl mice treated with pristane. The data were analyzed with one-way analysis of variance and Tukey's honestly significant difference tests. Results: The treatment with LXR or PPARγ/δ agonists did not significantly alter the swelling of lymph nodes, ds-DNA production, albuminuria, histological score of glomerular lesions, and mRNA expression of target genes including Abca1, C1qa, Icam1, Mertk and Tnf. Conclusion: LXR or PPARγ/δ agonists targeting the impaired clearance for apoptosis cells may not be efficient in the remission induction therapy in SLE.

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