Regional horizontal ecological compensation and ecosystem service value based on water resources pattern and insurance gain.

Ecological compensation plays an important role in maintaining ecosystem services and promoting regional green development. We built a regional horizontal ecological compensation model based on water resources pattern and insurance gain, and which was used to solve the problems of single compensation method and low compensation efficiency. Taking the Beijing-Tianjin-Hebei region as an example, we analyzed water footprint and water ecological carrying capacity from 2000 to 2019. The compensation subject and object and water footprint compensation amount were determined according to the input cost of ecological protection and allocation factor. Then, the insurance pricing model was introduced to determine ecological insurance premium rate. We calculated insurance compensation, ecological compensation standard and different types of ecosystem service value. Results showed that the whole region was at a state of water ecological deficit, with the agricultural water footprint accounting for 94.5%. From the perspective of the compensation subject and object, Beijing and Tianjin, as the compensation subject, needed to pay 0.402 billion yuan and 0.396 billion yuan (the amount of compensation) to Hebei Province each year. Hebei Province obtained a total of 0.228 billion yuan of ecological insurance with an insurance premium rate of 1.4%, and should receive an average annual ecological compensation standard of 0.81 billion yuan from Beijing and Tianjin. Hydrological regulation was the core ecosystem service in the region, with an average value of 187.974 billion yuan. It was of strategic significance to introduce ecological insurance mechanism to construct horizontal ecological compensation mechanism, improve ecosystem service function, and enhance the value of ecosystem services in the study area.

Neuroprotective effect of ß-asarone against Alzheimer's disease: regulation of synaptic plasticity by increased expression of SYP and GluR1.

AIM: ß-asarone, an active component of Acori graminei rhizome, has been reported to have neuroprotective effects in Alzheimer's disease. As the underlying mechanism is not known, we investigated the neuroprotective effects of ß-asarone in an APP/PS1 double transgenic mouse model and in NG108 cells. MATERIALS AND METHODS: APPswe/PS1dE9 double transgenic male mice were randomly assigned to a model group, ß-asarone treatment groups (21.2, 42.4, or 84.8 mg/kg/d), or donepezil treatment group (2 mg/kg/d). Donepezil treatment was a positive control, and background- and age-matched wild-type B6 mice were an external control group. ß-asarone (95.6% purity) was dissolved in 0.8% Tween 80 and administered by gavage once daily for 2.5 months. Control and model animals received an equal volume of vehicle. After 2.5 months of treatment, behavior of all animals was evaluated in a Morris water maze. Expression of synaptophysin (SYP) and glutamatergic receptor 1 (G1uR1) in the hippocampus and cortex of the double transgenic mice was assayed by Western blotting. The antagonistic effects of ß-asarone against amyloid-ß peptide (Aß) were investigated in vitro in the NG108-15 cell line. After 24 hours of incubation, cells were treated with 10 µm Aß with or without ß-asarone at different concentrations (6.25, 12.5, or 25 µM) for an additional 36 hours. The cytotoxicity of ß-asarone was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay of cell viability, and cell morphology was evaluated by bright-field microscopy after 24 hours of treatment. The expression of SYP and GluR1 in cells was detected by Western blot assay in the hippocampus and brain cortex tissues of mice. RESULTS: ß-asarone at a high dose reduced escape latency and upregulated SYP and GluR1 expression at both medium and high doses. Cell morphology evaluation showed that ß-asarone treatment did not result in obvious cell surface spots and cytoplasmic granularity. ß-asarone had a dose-dependent effect on cell proliferation. CONCLUSION: ß-asarone antagonized the Aß neurotoxicity in vivo, improved the learning and memory ability of APP/PS1 mice, and increased the expression of SYP and GluR1 both in vivo and in vitro. Thus, ß-asarone may be a potential drug for the treatment of Alzheimer's disease.