Figure 1.
Magnolol reduced glutamate-and N-methyl-D-aspartate (NMDA)-induced cell deaths.
(A, B) Differential interference contrast (DIC) photomicrographs showed neurotoxicity of magnolol at a concentration beyond 100 µM. (C, D) Magnolol (0.1–1 µM) achieved potent cytoprotection against glutamate-induced neuronal damage. (E) Magnolol (0.1–1 µM) achieved potent cytoprotection against NMDA-induced neuronal damage. *P<0.05 vs controls, and n = 5–9 per group.
Figure 2.
Magnolol attenuated glutamate-induced rises in the intracellular calcium, [Ca2+](i), inflow and cell swelling in cultured neurons.
(A) Ratio image detection for [Ca2+](i) concentrations showed that magnolol at 0.1 µM, but not at 0.01 and 1 µM, effectively inhibited the rises of [Ca2+](i) induced by glutamate exposure. (B) Time-course differential interference contrast (DIC) photomicrographs of cultured neurons showed that magnolol at 0.1–1 µM attenuated the glutamate-induced cell swelling over time. *P<0.05 vs controls, and n = 6–7 per group.
Table 1.
Physiologic parameters before (preocclusion) and after (postocclusion) permanent middle cerebral artery occlusion (PMCAO) between animals pretreated with magnolol versus vehicle (PEG 400)-treated controls.
Table 2.
The changes of core temperatures obtained after vehicle or magnolol treatment in rats subjected to permanent middle cerebral artery occlusion (PMCAO) in the study.
Figure 3.
Magnolol reduced brain infarction in rats subjected to permanent middle cerebral artery (pMCAO) occlusion.
Animals which were subjected to pMCAO and received an intraperitoneal injection of PEG 400 (n = 15) or magnolol, at 25 mg/kg (n = 13), 50 mg/kg (n = 11), 100 mg/kg (n = 8), 150 mg/kg (n = 9), or 200 mg/kg (n = 12), 1 hr before the ischemic insult. Infarct volumes were significantly reduced with magnolol treatment at 50–200 mg/kg (A), but not at 25 mg/kg. (B) The 2, 3, 5-Triphenyltetrazolium chloride (TTC)-stained coronal sections were from representative animals which received an intraperitoneal injection of PEG 400 or magnolol (100 mg/kg), at 4 hrs post-insult. Infarcts observed (pale region) involving the cerebral cortex and underlying striatum are substantially smaller in the magnolol-treated group. (C) Delayed treatment with magnolol (100 mg/kg) at 1 (n = 7), 2 (n = 7), or 4 hrs (n = 9), but not 6 hrs (n = 9), significantly reduced brain infarction, compared to controls (n = 30). The infarct volumes are expressed as a percentage of the contralateral hemisphere. *P<0.05 vs PEG 400-treated rats. n, number of animals.
Table 3.
Neurobehavioral scores and body weight loss obtained after permanent middle cerebral artery occlusion (pMCAO) in each pretreatment group in the study.