[Construction on the chitosan microparticles of baicalin and comparison of transdermal diffusion in vitro of baicalin in chitosan microparticles and cream].

OBJECTIVE: To construct baicalin chitosan microparticles and compare the in vitro transdermal diffusion of baicalin in microparticles and cream. METHODS: Baicalin chitosan microparticles were constructed by using neutralization method and optimized by orthogonal test; The in vitro transdermal diffusion of baicalin in microparticles and cream was compared by using Franz cell. RESULTS: When the drug:stuff ratio was 1:3, concentration of chitosan was 2 mg/mL, mixed duration was 10 min, both the entrapment efficiency and drug loading efficiency of baicalin chitosan microparticles were over 60%; After 36 h, the cumulative release percentage of baicalin in microparticles and cream in vitro transdermal diffusion was 4.04% and 30%, respectively. The content of drug in microparticles and cream in the skin was 0.11% and 0.14%, respectively. And there was no significant difference (w = 7, P = 0.127) between the content of drug in microparticles and cream in the skin. CONCLUSION: The optimal procedure is simple and convenient with high entrapment efficiency and drug loading efficiency. The drug in the microparticles could be released slower and form local drug reservoir in the skin.

[Effects of Microplastics on Membrane Fouling During a Shortened Ultrafiltration Membrane Process].

Microplastics have garnered much attention worldwide as a new emerging pollutant. As they are gradually detected in freshwaters, understanding how microplastics will behave during current drinking water treatment processes is urgently needed. In recent years, the shortened process with an ultrafiltration (UF) membrane has shown excellent performance because of its low land use and high water purification efficiency. In this work, the membrane performance induced by microplastics was investigated with a shortened UF membrane process. The results showed that membrane fouling was always induced by the cake layer before and after coagulating with microplastics. Owing to the small UF membrane pore size (d<0.1 µm), slight membrane fouling was caused by microplastics (d<5 mm) alone. However, although the loose cake layer was formed because of the existence of flocs, the cyberspace formed by flocs was easily entered by small microplastics with increasing coagulant dosage. As a result, server membrane fouling was induced because of the formation of a dense cake layer. It was shown that the specific membrane flux induced by flocs alone was 0.82 and 0.76 in the presence of 0.1 mmol·L-1 and 0.9 mmol·L-1 FeCl3·6H2O, respectively. However, after coagulation the specific membrane fouling induced by the 0.1 g small microplastics (d<0.5 mm) was 0.76 and 0.62 with 0.1 mmol·L-1 and 0.9 mmol·L-1 FeCl3·6H2O, respectively. In addition, microplastics were always negatively charged in water. In comparison with alkaline conditions, Fe-based flocs were positively charged under acidic conditions, which were also much smaller. Therefore, microplastics were more easily adsorbed by Fe-based flocs under acidic conditions, leading to severe membrane fouling because of the dense cake layer formed. After coagulating with 0.3 mmol·L-1 FeCl3·6H2O, the specific membrane flux induced by 0.1 g small microplastics (d<0.5 mm) was 0.55 and 0.79 at pH 6.0 and 8.0, respectively.

Pretreatment with Sodium Phenylbutyrate Alleviates Cerebral Ischemia/Reperfusion Injury by Upregulating DJ-1 Protein.

Oxidative stress and mitochondrial dysfunction play critical roles in ischemia/reperfusion (I/R) injury. DJ-1 is an endogenous antioxidant that attenuates oxidative stress and maintains mitochondrial function, likely acting as a protector of I/R injury. In the present study, we explored the protective effect of a possible DJ-1 agonist, sodium phenylbutyrate (SPB), against I/R injury by protecting mitochondrial dysfunction via the upregulation of DJ-1 protein. Pretreatment with SPB upregulated the DJ-1 protein level and rescued the I/R injury-induced DJ-1 decrease about 50% both in vivo and in vitro. SPB also improved cellular viability and mitochondrial function and alleviated neuronal apoptosis both in cell and animal models; these effects of SPB were abolished by DJ-1 knockdown with siRNA. Furthermore, SPB improved the survival rate about 20% and neurological functions, as well as reduced about 50% of the infarct volume and brain edema, of middle cerebral artery occlusion mice 23 h after reperfusion. Therefore, our findings demonstrate that preconditioning of SPB possesses a neuroprotective effect against cerebral I/R injury by protecting mitochondrial function dependent on the DJ-1 upregulation, suggesting that DJ-1 is a potential therapeutic target for clinical ischemic stroke.