Protective effects of IGF-1 on cell injuries and tau hyperphosphorylation induced by okadaic acid / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To investigate the effects of insulin-like growth factor-1 (IGF-1) on cell injuries and tau hyperphosphorylation induced by okadaic acid (OA).</p><p><b>METHODS</b>The experimental groups were designed as follows: (1) SH-SY5Y culture (control group); (2) SH-SY5Y exposed to 40 nmol/L OA for 24 hours (OA group); (3) SH-SY5Y exposed to OA for 24 hours in the presence of 2 hour pretreatment with 100, 200 and 400 ng/ml IGF-1 (IGF-1 pretreatment groups). The changes of cell morphology were observed by inverted microscope. The viability of cells was detected by MTT. The injuries of cells were examined by Hoechst 33258 staining and the activity of caspase-3. Western-blot was applied to determine the expression of phosphorylation of tau protein.</p><p><b>RESULTS</b>In IGF-1 pretreatment group, the cell morphology was improved, the viability of cells was increased, and caspase-3 activation and hyperphosphorylation of tau (Ser396) were reduced.</p><p><b>CONCLUSION</b>IGF-1 can protect the SH-SY5Y cells from cell injuries induced by OA by inhibiting tau hyperphosphorylation.</p>

Melatonin enhances the expression of β-endorphin in hypothalamic arcuate nucleus of morphine-dependent mice / 生理学报

The study was conducted to investigate the effect of melatonin (MEL) on the expression of β-endorphin (β-EP) in the hypothalamic arcuate nucleus (ARH) of morphine-dependent mice. For a period of 8 consecutive days, male Kunming strain mice were injected subcutaneously (s.c.) with normal saline or increasing doses (10-80 mg/kg) of morphine, and intraperitoneally (i.p.) with MEL (10, 20 or 40 mg/kg) or vehicle (5% ethanol saline) simultaneously. Withdrawal response was induced by naloxone (3 mg/kg, s.c.) at 2 h after final morphine injection on the 8th day. The potency of withdrawal response was evaluated according to the jumping times and the body weight loss. After that, the expressions of β-EP and proopiomelanocortin (POMC) mRNA in ARH were examined by immunohistochemistry and RT-PCR, respectively. The results showed that MEL (i.p., 20 mg/kg) decreased the naloxone-precipitated withdrawal responses in morphine-dependent mice significantly (P<0.05). Meanwhile, MEL increased the intensity of β-EP-like immunoreactivity and enhanced the expression of POMC mRNA in ARH (P<0.05). These results suggest that MEL increases the expression of β-EP in ARH of morphine-dependent mice, which may partly contribute to the action of MEL to inhibit the development of morphine dependence.

Effect of melatonin on the content of β-endorphin in the hypothalamic arcuate nucleus and periaqueductal grey of midbrain in morphine withdrawal mice / 生理学报

The present study was undertaken to investigate the effect of melatonin on the content of β-endorphin (β-EP) in the hypothalamic arcuate nucleus (Arc) and periaqueductal grey (PAG) of midbrain in morphine withdrawal mice. Male Kunming mice were injected subcutaneously (s.c.) with an increasing dose of morphine continuously for 8 d to establish morphine dependence model. Withdrawal response was induced by naloxone (3 mg/kg body weight, s.c.). The potency of withdrawal response was evaluated according to the jumping times and body weight loss. Ninty minutes prior to the precipitation of naloxone, 80 mg/kg body weight of melatonin (MEL) was injected intraperitoneally (i.p.) to observe its antagonistic effect on the withdrawal response in morphine-dependent mice. After behavioral observation, radioimmunoassay was used to determine the content of β-EP in the PAG of midbrain, and immunohistochemical assay was used to observe the intensity of β-EP-like immunoreactivity in the Arc in mice. It was shown that MEL inhibited the naloxone-precipitated withdrawal responses in mice significantly (P<0.05). In the meantime, MEL increased the content of β-EP in the PAG of midbrain significantly (P<0.05) and attenuated the intensity of β-EP-like immunoreactivity in the Arc in mice (P<0.05). The results suggest that MEL increases the content of β-EP in the PAG of midbrain, decrease the content of β-EP in the Arc in morphine withdrawal mice.

Effect of melatonin on learning and memory impairment induced by aluminum chloride and its mechanism / 药学学报

<p><b>AIM</b>To investigate the effect of melatonin on learning and memory impairment in mice induced by aluminum chloride and its possible mechanism.</p><p><b>METHODS</b>Mice were treated with intracerebroventricular (icv) injection of 2 microL 5% aluminum chloride solution, once a day for 5 d. At the same time, the mice were given intraperitoneally melatonin 0.6, 3 and 15 mg.kg-1, once a day for 14 d. The passive avoidance of the mice was assessed by step-through test on day 15 after the last icv injection, and then the place navigation and spatial probe ability by Morris water maze were tested. After the spatial probe test, the activities of total superoxide dismutase (T-SOD), CuZn superoxide dismutase (CuZn-SOD), glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA) in the cerebral cortex and hippocampus of mice brain were determined.</p><p><b>RESULTS</b>Melatonin ameliorated significantly the impairment of passive avoidance memory, the place navigation and spatial probe ability of mice induced by aluminum chloride. Melatonin was found to prevent significantly the decline of T-SOD, CuZn-SOD and GSH-Px activities, the increase of MDA content in the cortex and hippocampus of mouse brain induced by aluminum chloride.</p><p><b>CONCLUSION</b>The results suggest that melatonin improves significantly the learning and memory impairment in mice induced by aluminum chloride, and this effect may be attributed to its antioxidation.</p>