Ginsenoside Rg1 is the main active ingredient of Panax ginseng with the activity of neuroprotective, antioxidant and strengthening the immune system. Therefore, we hypothesized that Rg1 may afford anti-aging effects although the mechanism remains to be elucidated. In this study, chemically induced aging mice were established by consecutive administration of D-galactose and AlCl3. We found that Rg1 effectively ameliorates spatial learning and memory deficits in aging mice demonstrated by their improved performance in step down avoidance tests and Morris water maze experiments. Rg1 restored aging-induced decline of FGF2 and BDNF, reactivated TrkB/Akt signaling pathways in the hippocampus and prefrontal cortex to inhibit apoptosis, for the expression of anti-apoptotic protein Bcl-2 and apoptosis promoting enzyme cleaved-Caspase3 were antagonistically restored. Therefore, these results established the anti-aging effects of Rg1, and FGF2, BDNF and associated signaling pathways might be promising targets. Our data may provide a new avenue to the pharmacological research and diet therapeutic role of ethnic products such as Rg1 in anti-aging and aging associated diseases.

2,3,5,4′-Tetrahydroxystilbene-2-O-β-d-glucoside (THSG) affords neuroprotective effects against MPP+-induced neurotoxicityin vitroandin vivoby restoring the BDNF-TrkB and FGF2-Akt signaling axis to inhibit apoptosis and promote cell survival.

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Exportin 1 (XPO1) is an important transport receptor that mediates the nuclear export of various proteins and RNA. KPT-8602 is a second-generation inhibitor of XPO1, demonstrating the lowest level of side effects, and is currently in clinical trials for the treatment of cancers. Previous studies suggest that several first-generation inhibitors of XPO1 demonstrate anti-inflammation activities, indicating the application of this drug in inflammation-related diseases. In this study, our results suggested the potent anti-inflammatory effect of KPT-8602 in vitro and in vivo. KPT-8602 inhibited the activation of the NF-κB pathway by blocking the phosphorylation and degradation of IκBα, and the priming of NLRP3. Importantly, the administration of KPT-8602 attenuated both lipopolysaccharide (LPS)-induced peripheral inflammation and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neuroinflammation in vivo. In addition, the tissue damage was also ameliorated by KPT-8602, indicating that KPT-8602 could be used as a novel potential therapeutic agent for the treatment of inflammasome-related diseases such as Parkinson’s disease, through the regulation of the NF-κB signaling pathway and the NLRP3 inflammasome.

For this paper, GREENSPAN sap flow system was used to monitor the dynamics of trunk sap flow of Gingkgo biloba. Results indicate that sap flow velocity is significantly different among different heights, depths, and directions of the trunk. Sap flow velocity at the upper position of the trunk is higher than that of the middle and lower position, but cumulative flux is not significantly different among the upper, middle and lower sections. Sap flow velocity at 10 mm reached the most and that at 20 mm the least. However, sap flow velocity at 5 mm and 15 mm was similar and was second among the four depths. Results also showed that sap flow velocity of the south was the highest, and that of the west was next. An Automatic Weather Station of HOBO was synchronously applied to measure these meteorological parameters, and the relationship between these parameters and the changes of trunk sap flow velocity were analyzed. We found that the change of sap flow velocity was a single-crest curve on clear days and multi-crest curve on cloudy and rainy days. In addition, it is also revealed that by stepwise regression analyses photosynthetical active radiation (PAR), temperature and wind speed are the main environmental factors affecting sap flow velocity. The efficient methods of reducing water transpiration of trees, including leaf pruning, overshadowing and antitranspirant spraying, were found by investigating the effects on inhibiting transpiration, which indicated that spraying of antitranspirants, leaf pruning and overshadowing could significantly reduce transpiration but the effects of leaf pruning and overshadowing were far better than that of antitranspirant spraying.

MicroRNAs (miRNAs) are small non-coding RNAs with the unique ability to degrade or block specific RNAs and regulate many cellular processes. Neuroinflammation plays the pivotal role in the occurrence and development of multiple central nervous system (CNS) diseases. The ability of miRNAs to enhance or restrict neuroinflammatory signaling pathways in CNS diseases is an emerging and important research area, including neurodegenerative diseases, stroke, and traumatic brain injury (TBI). In this review, we summarize the roles and regulatory mechanisms of recently identified miRNAs involved in neuroinflammation-mediated CNS diseases, aiming to explore and provide a better understanding and direction for the treatment of CNS diseases.

Background: Neuroinflammation is involved in the development of Parkinson's disease (PD). Calhm2 plays an important role in the development of microglial inflammation, but whether Calhm2 is involved in PD and its regulatory mechanisms are unclear. Methods: To study the role of Calhm2 in the development of PD, we utilized conventional Calhm2 knockout mice, microglial Calhm2 knockout mice and neuronal Calhm2 knockout mice, and established the MPTP-induced PD mice model. Moreover, a series of methods including behavioral test, immunohistochemistry, immunofluorescence, real-time polymerase chain reaction, western blot, mass spectrometry analysis and co-immunoprecipitation were utilized to study the regulatory mechanisms. Results: We found that both conventional Calhm2 knockout and microglial Calhm2 knockout significantly reduced dopaminergic neuronal loss, and decreased microglial numbers, thereby improving locomotor performance in PD model mice. Mechanistically, we found that Calhm2 interacted with EFhd2 and regulated downstream STAT3 signaling in microglia. Knockdown of Calhm2 or EFhd2 both inhibited downstream STAT3 signaling and inflammatory cytokine levels in microglia. Conclusion: We demonstrate the important role of Calhm2 in microglial activation and the pathology of PD, thus providing a potential therapeutic target for microglia-mediated neuroinflammation-related diseases.