Dendrobium polysaccharides attenuate cognitive impairment in senescence-accelerated mouse prone 8 mice via modulation of microglial activation.

Dendrobium is one of the most important traditional Chinese medicinal foods used to treat age-related disorders. However, it remains unclear whether Dendrobium affects the progression of Alzheimer's disease (AD). In the present study, we investigated the effects of Dendrobium officinale polysaccharides (DOP) on the BV2 microglial cell line and the senescence-accelerated mouse prone 8 (SAMP8) mouse strain. In vitro experiments showed that DOP pretreatment contributed to BV2 cells shifting from proinflammatory to anti-inflammatory phenotypes with enhanced Aß clearance in response to Aß insults. For the in vivo study, mice were chronically treated with DOP in drinking water from 4 to 7 months of age. The results showed that DOP remarkably attenuated cognitive decline in SAMP8 mice. DOP also inhibited the increased hippocampal microglial activation in SAMP8 mice with downregulation of interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), while interleukin-10 (IL-10), neprilysin (NEP) and insulin-degrading enzyme (IDE) were upregulated. The accumulation of hippocampal Aß42 and phosphated Tau proteins in SAMP8 mice was also reduced. Taken together, our data suggest that Dendrobium has the potential to provide neuroprotection against AD-related cognitive impairment via modulation of microglial activation.

Huanglian-Jie-Du-Tang Extract Ameliorates Depression-Like Behaviors through BDNF-TrkB-CREB Pathway in Rats with Chronic Unpredictable Stress.

Neuroinflammation is considered as one of the common pathogeneses of depression. Huanglian-Jie-Du-Tang (HJDT) is a traditional Chinese herbal formula. The present study investigates the antidepressant-like effect of HJDT and its possible mechanism in rats. Rats were given HJDT (2, 4, and 8 g/kg, intragastrically), paroxetine (1.8 mg/kg, intragastrically), or an equivalent volume of saline for 42 days. The depression-related behaviors, including sucrose preference test (SPT), open field test (OFT), novel objective recognition task (NORT), and forced swimming test (FST), were detected. 5-Hydroxytryptamine (5-HT) and dopamine (DA) contents, microglial activation, proinflammatory cytokines, and brain derived neurotrophic factor (BDNF), tropomyosin receptor kinases B (TrkB), and cAMP-responsive element binding protein (CREB) expression were investigated. The results indicated HJDT (2 and 4 g/kg) dramatically ameliorated the depression-like behaviors. Also HJDT decreased the number of microglia and the proinflammatory cytokines in hippocampus. Western-blotting analysis displayed HJDT upregulated BDNF, TrkB, and pCREB/CREB expression in hippocampus. Particularly, pCREB DNA activity enhanced with HJDT treatment in hippocampus. But there was no difference in the 5-HT and DA contents with HJDT treatment. In conclusion, it was supposed that HJDT might be a potential Chinese medicine decoction for treating or alleviating complex symptoms of depression through BDNF-TrkB-CREB pathway.

[Screening of Active Fractions from Huanglian Jiedu Decoction against Primary Neuron Injury after Oxygen-Glucose Deprivation].

OBJECTIVE: To observe the protective effect of active fractions of Huanglian Jiedu Decoction (HJD) on primary cortical neuron injury after oxygen-glucose deprivation (OGD)/reperfusion (R) injury. Methods Using macroporous resin method, HJDFE30, HJDFE50, HJDFE75, and HJDFE95 with 30%, 50%, 75%, and 95% alcohol were respectively prepared. Then the content of active components in different HJD fractions was determined with reverse phase high-performance liquid chromatography (RP-HPLC). The OGD/R injury model was induced by sodium dithionite on primary cortical neurons in neonate rats. MTT assay was used to observe the effect of four fractions (HJDFE30, HJDFE50, HJDFE75, and HJDFE95) and seven index components of HJD on the neuron viability. RESULTS: RP-HPLC showed active component(s) contained in HJDFE30 was geniposide; baicalin, palmatine, berberine, and wogonside contained in HJDFE50; baicalin, berberine, baicalein, and wogonin contained in HJDFE75. The neuron viability was decreased after OGD for 20 min and reperfusion for 1 h, (P <0. 01), and significantly increased after administered with HJD, HJDFE30, HJDFE50, and HJDFE75 (P <0. 05, P <0. 01). Geniposide, baicalin, baicalein, palmatine, wogonside, and wogonin could increase the cortical neuron viability (P <0. 05, P <0. 01). CONCLUSIONS: HJDFE30, HJDFE50, and HJDFE75, as active fractions of HJD, had protective effect on primary cortical neuron injury after OGD/R. Furthermore, geniposide, baicalin, and baicalein were main active components of HJD.

[Protective effects of Huanglian-Jiedu-Tang on chronic brain injury after focal cerebral ischemia in mice].

OBJECTIVE: To investigate the neuroprotective effects of Chinese herb medicine Huanglian-Jiedu-Tang (HJDT) on chronic brain injury after focal cerebral ischemia in mice. METHODS: Focal cerebral ischemia was induced by occlusion of right middle cerebral artery (MCA) for 15 min. HJDT (at dosage of 2 g/kg or 4 g/kg, qd, orally) was administered for 21 d from d 7 before ischemia until d 14 after ischemia. The sham and ischemic controls were administered with normal saline orally. The neurological deficit scoring and the inclined board testing were performed within 35 d after ischemia. The survival rate, the infarct volume and the neuron density were assessed 35 d after ischemia. RESULT: HJDT increased the survival rate at dose of 4 g/kg; significantly reduced the neurological deficits, infarct volume and cerebral atrophy at doses of 2 and 4 g/kg after ischemia; and significantly increased the neuron density in the ischemic hippocampal CA1 region, striatum and cortex at dose of 4 g/kg but only increase the density in hippocampal CA1 region at dose of 2 g/kg. CONCLUSION: Chinese herb medicine HJDT has neuroprotective effects on chronic brain injury after focal cerebral ischemia in mice.