Curcumin reverses corticosterone-induced depressive-like behavior and decrease in brain BDNF levels in rats.

A rat model of depression has been recently developed using exogenous corticosterone (CORT) administration. This study aimed to examine the antidepressant-like effect and the possible mechanisms of curcumin in a CORT-induced depression model in rats. The results showed that 3-week CORT injections caused depression-like behavior in rats, as indicated by the significant decrease in sucrose consumption and increase in immobility time in the forced swim test. Repeated CORT injections also significantly decreased brain-derived neurotrophic factor (BDNF) protein levels in the hippocampus and frontal cortex of the rats. Treatment of the rats with curcumin significantly suppressed the depression-like behavior and the decrease in brain BDNF levels induced by the repeated CORT injections. The results suggest that curcumin produces an antidepressant-like effect in CORT-treated rats, which is possibly mediated by increasing BDNF expression in the hippocampus and frontal cortex.

Herbal formula SYJN increases neurotrophin-3 and nerve growth factor expression in brain regions of rats exposed to chronic unpredictable stress.

AIM OF THE STUDY: SYJN is a Chinese herbal formula that contains four herbs: Bupleurum chinense DC., Curcuma aromatica Salisb., Perilla frutescens (L.) Britt., and Acorus tatarinowii Schott. Previous studies conducted in our laboratory have revealed an antidepressant-like effect of the formula in chronic unpredictable stress (CUS)-induced depression model in rats. The present study aimed to investigate whether neurotrophin-3 (NT-3) and nerve growth factor (NGF) are involved in the antidepressant-like action of SYJN by using the same depressive model in rats. MATERIALS AND METHODS: Rats were subjected to an experimental setting of CUS. The mechanism underlying the antidepressant-like action of SYJN was examined by measuring protein and mRNA expression of NT-3 and NGF in brain tissues of CUS-exposed rats. RESULTS: The results showed that NT-3 protein and mRNA expression in the hippocampus and frontal cortex were significantly decreased in CUS-treated rats. CUS treatment also significantly decreased NGF protein and mRNA expression in the frontal cortex of the animals. Daily intragastric administration of SYJN (1300 or 2600 mg/kg/day) during the 4 weeks of CUS significantly suppressed these changes induced by CUS. CONCLUSION: The results suggest that the antidepressant-like activity of SYJN is likely mediated by the increases in NT-3 and NGF expression in brain tissues.

Protective effects of paeoniflorin against glutamate-induced neurotoxicity in PC12 cells via antioxidant mechanisms and Ca(2+) antagonism.

Preclinical and clinical investigations have shown hippocampal neuronal atrophy and destruction were observed in patients with depression, which could be ameliorated by the treatment with antidepressants. Therefore, neuroprotection has been proposed to be one of the acting mechanisms of antidepressant. Paeoniflorin, a monoterpene glycoside, has been reported to display antidepressant-like effects in animal models of behavioral despair. The present study aimed to examine the protective effect of paeoniflorin on glutamate-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. The results showed that pretreatment with paeoniflorin elevated cell viability, inhibited apoptosis, decreased levels of intracellular reactive oxygen species and malondialdehyde, and enhanced activity of superoxide dismutase in glutamate-treated PC12 cells. Pretreatment with paeoniflorin also reversed the increased intracellular Ca(2+) concentration and the reduced Calbindin-D28K mRNA level caused by glutamate in PC12 cells. The results suggest that paeoniflorin exerts a neuroprotective effect on glutamate-induced neurotoxicity in PC12 cells, at least in part, via inhibiting oxidative stress and Ca(2+) overload. This neuroprotective effect may be one of the action pathways accounting for the in vivo antidepressant activity of paeoniflorin.

Effects of SYJN, a Chinese herbal formula, on chronic unpredictable stress-induced changes in behavior and brain BDNF in rats.

AIM OF THE STUDY: Suyu-Jiaonang (SYJN) is a Chinese herbal formula that contains four herbs: Bupleurum chinense DC, Curcuma aromatica Salisb., Perilla frutescens (Linn.) Britt., and Acorus tatarinowii Schott. Previous studies conducted in our laboratory have revealed an antidepressant-like effect of the formula in various mouse models of behavioral despair. The present study aimed to investigate whether SYJN could produce antidepressant-like effects in chronic unpredictable stress (CUS)-induced depression model in rats and its possible mechanism(s). MATERIALS AND METHODS: Rats were subjected to an experimental setting of CUS. The effect of SYJN treatment on CUS-induced depression was examined using behavioral tests including the sucrose consumption and open field tests. The mechanism underlying the antidepressant-like action of SYJN was examined by measuring brain-derived neurotrophic factor (BDNF) protein and mRNA expression in brain tissues of CUS-exposed rats. RESULTS: Exposure to CUS for 4 weeks caused depression-like behavior in rats, as indicated by significant decreases in sucrose consumption and locomotor activity (assessed in the open field test). In addition, it was found that BDNF protein and mRNA levels in the hippocampus and frontal cortex were lower in CUS-treated rats, as compared to controls. Daily intragastric administration of SYJN (1300 or 2600 mg/kg) during the 4-week period of CUS significantly suppressed behavioral changes and attenuated the CUS-induced decrease in BDNF protein and mRNA levels in the hippocampus and frontal cortex. CONCLUSION: The results suggest that SYJN alleviates depression induced by CUS. The antidepressant-like activity of SYJN is likely mediated by the increase in BDNF expression in brain tissues.

Herbal formula SYJN protect PC12 cells from neurotoxicity induced by corticosterone.

AIM OF THE STUDY: SYJN is a Chinese herbal formula, containing four herbs: Bupleurum chinense DC., Curcuma aromatica Salisb., Perilla frutescens (Linn.) Britt. and Acorus tatarinowii Schott. Previous studies on the formula in our laboratory revealed an antidepressant-like effect on animal models of behavioral despair. However,the mechanisms underlying such antidepressant-like effect are yet to be understood. The aim of this work was to verify the previously established antidepressant-like effects on cell level using corticosterone-induced neurotoxicity in rat pheochromocytoma (PC12) cells to see if SYJN possesses any neuroprotective properties. MATERIALS AND METHODS: PC12 cells were treated with 200 microM corticosterone in the absence or the presence of various concentrations of SYJN for 48 h. Then, cell viability, apoptosis, intracellular Ca(2+) ([Ca(2+)]i) concentration and caspase-3 activity were determined. RESULTS: Following the exposure of PC12 cells to 200 microM corticosterone for 48 h, there were reductions in cell survival rate but increases in lactate dehydrogenase (LDH) release. In parallel, corticosterone caused significant elevations in DNA fragmentation, [Ca(2+)]i concentration and caspase-3 activity. However, when the PC12 cells were incubated with SYJN at different concentrations (10, 50 and 100mg/L) in the presence of 200 microM corticosterone for 48 h, the above effects were evidently alleviated in a dose-dependent manner. CONCLUSION: SYJN could generate a neuroprotective effect on corticosterone-induced neurotoxicity in PC12 cells, suggesting a possible action pathway of SYJN in vivo by decreasing the [Ca(2+)]i concentration and caspase-3 activity.