Pickering emulsion, a kind of emulsion stabilized only by solid particles locating at oil-water interface, has been discovered a century ago, while being extensively studied in recent decades. Substituting solid particles for traditional surfactants, Pickering emulsions are more stable against coalescence and can obtain many useful properties. Besides, they are more biocompatible when solid particles employed are relatively safe in vivo. Pickering emulsions can be applied in a wide range of fields, such as biomedicine, food, fine chemical synthesis, cosmetics and so on, by properly tuning types and properties of solid emulsifiers. In this article, we give an overview of Pickering emulsions, focusing on some kinds of solid particles commonly serving as emulsifiers, three main types of products from Pickering emulsions, morphology of solid particles and as-prepared materials, as well as applications in different fields.

Background: Idebenone is an antioxidant and a coenzyme Q10 analog that has been used to treat neurodegeneration disease. Some studies show idebenone exerts anti-inflammatory effects. However, whether idebenone can be used to reduce the neuroinflammation in Parkinson’s disease (PD) has been little studied. Methods: The study investigated the potential anti-inflammatory effects of idebenone in vitro and in vivo, using cell models of Lipopolysaccharide (LPS)-simulated BV2 cells and animal models of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD with or without idebenone. To verify how idebenone exerts its effects on the BV2 cell activation and PD model, we performed the mechanistic studies in vitro and in vivo. Results: In vitro study showed that pretreatment with idebenone could attenuate the production of pro-inflammatory factors in LPS-stimulated BV2 cells and promoted a phenotypic switch from the M1 state to the M2 state. Mechanistically, idebenone reduced the activation of the MAPK and NF-κB signaling pathway upon LPS stimulation. Furthermore, in vivo experiments confirmed that pretreatment with idebenone could ameliorate MPTP-induced neurodegeneration and modulate microglia phenotypes through inhibition of the MAPK and NF-κB signaling pathway in the SN. Conclusion: These results suggest that idebenone ameliorates the neurological deficits related to PD and this effect is partly mediated by inhibiting the neuroinflammation and modulating microglia phenotypes.

Parkinson’s disease (PD) is a chronic, progressive and debilitating disease, which affects over 2.5 million people in China. PD is characterized clinically by resting tremor, muscular rigidity, bradykinesia and postural instability. As the disease progresses, additional complications can arise such as non-motor and neurobehavioral symptoms. Pharmacological treatment and surgical intervention for PD have been implemented in China. Until 10 years ago, there was lack of standardization for the management of PD in different regions and among different physicians, leading to different treatment levels in different regions and different physicians. Since then, the Chinese Parkinson’s Disease and Movement Disorder Society have published three versions of guidelines for the management of PD in China, in 2006, 2009 and 2014, respectively. Correspondingly, the overall level of treatment for PD in China improved. To update the treatment guidelines based on current foreign and domestic practice guidelines and clinical evidence, and to improve the treatment options available to physicians in the management of PD. A variety of treatment recommendations in the treatment guidelines have been proposed, including physical activity and disease-modifying medication, which should be initiated at the early-stage of the disease. The principles of dosage titration should be followed to avoid acute adverse reactions to the drugs, to achieve a satisfactory clinical effect with a low dose and to reduce the incidence of long-term motor complications. Moreover, different treatment strategies should be considered at different stages of the disease. Importantly, treatment guidelines and personalized treatments should be valued equally. A set of treatment recommendations has been developed to assist physicians to improve and optimize clinical outcomes for patients with PD in China.

Lipopolyplex is a core-shell structure composed of nucleic acid, polycation and lipid. As a non-viral gene delivery vector, lipopolyplex combining the advantages of polyplex and lipoplex has shown superior colloidal stability, reduced cytotoxicity, extremely high gene transfection efficiency. Following intravenous administration, there are many strategies based on lipopolyplex to overcome the complex biological barriers in systemic gene delivery including condensation of nucleic acids into nanoparticles, long circulation, cell targeting, endosomal escape, release to cytoplasm and entry into cell nucleus. Parkinson’s disease is the second most common neurodegenerative disorder and severely influences the patients’ life quality. Current gene therapy clinical trials for Parkinson’s disease employing viral vectors didn’t achieve satisfactory efficacy. However, lipopolyplex may become a promising alternative approach owing to its stability in blood, ability to cross the blood-brain barrier and specific targeting to diseased brain cells.

Background: Neuroinflammation plays an important role in the pathogenesis of Parkinson's disease (PD). Inflammatory cytokines in the peripheral immune system can induce neuroinflammation in central nervous system (CNS). Whether the peripheral immune system is involved in PD is unclear. The present study investigated the contribution of the peripheral immune system to the neuronal loss in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP) model of PD. Methods: MPTP was intraperitoneally injected into mice to generate a PD model. Mice received clodronate liposomes every 3 days to deplete peripheral macrophages. The percentages of macrophages were measured by flow cytometry at 1, 3, and 7 days after MPTP injection. Neurobehavioral parameters, protein expression, inflammatory cytokines release, and microglia activation were measured by the open field test, western blotting, quantitative polymerase chain reaction (qPCR), and immunofluorescence staining, respectively at 7 days after MPTP injection. Results: Our study revealed that intraperitoneal injection of MPTP could increase peripheral M1 macrophages levels. It also can induce T cells infiltration and cytokine release. Depletion of M1 macrophages by clodronate liposomes suppressed these inflammatory effects and blunted the loss of TH+ nigral neurons and functional impairments caused by MPTP. Conclusion: Our results indicated the critical role of M1 macrophages in the pathogenesis of PD and proposed inhibition of M1 macrophages as a promising therapeutic approach for neurodegeneration.

The neuroprotective actions of Ginsenoside-Rg1 (G-Rg1) have been documented for experimental stroke therapy. We used a systematic review and meta-analysis to assess the efficacy of G-Rg1 in experimental ischemic stroke. We identified studies describing the efficacy of G-Rg1 in animal models of focal cerebral ischemia. Primary outcomes were infarct volume and neurological function score (NFS). In all, eleven studies reported significant effects of G-Rg1 for improving the NFS when compared with the control group (P < 0.00001), and four studies reported significant effects of G-Rg1 for reducing infarct volume compared with middle cerebral artery occlusion group (P < 0.00001). Meanwhile, studies reported G-Rg1 was more efficacious than positive control drug nimodipine (0.7 or 1 mg/kg, intraperitoneal) according to NFS (P = 0.009) and infarct volume (p = 0.0002). The results demonstrate a marked efficacy of G-Rg1 in experimental acute ischemic stroke, but raise concerns that our value of effect size might be overestimate due to factors such as study quality and possible publication bias. Even so, the findings suggest G-Rg1 as a candidate neuroprotective drug for human ischemic stroke.