ABSTRACT
Motion is influenced by many different aspects of a micromotor's design, such as shape, roughness and the type of materials used. When designing a motor, asymmetry is the main requirement to take into account, either in shape or in catalyst distribution. It influences both speed and directionality since it dictates the location of propulsion force. Here, we combine asymmetry in shape and asymmetry in catalyst distribution to study the motion of soft micromotors. A microfluidic method is utilized to generate aqueous double emulsions, which upon UV-exposure form asymmetric microgels. Taking advantage of the flexibility of this method, we fabricated micromotors with homogeneous catalyst distribution throughout the microbead and micromotors with different degrees of catalyst localization within the active site. Spatial control over catalyst positioning is advantageous since less enzyme is needed for the same propulsion speed as the homogeneous system and it provides further confinement and compartmentalization of the catalyst. This proof-of-concept of our new design will make the use of enzymes as driving forces for motors more accessible, as well as providing a new route for compartmentalizing enzymes at interfaces without the need for catalyst-specific functionalization.
ABSTRACT
Recent studies have demonstrated that hydrogen sulfide (H2S) has a neuroprotective effect in neurodegenerative diseases. It is possible that this effect is supported by brain-derived neurotrophic factor (BDNF). Our aim is to examine the effects of H2S on neural damage in Parkinson's disease (PD) and to reveal the role of the BDNF-TrkB pathway in its possible effect. PD model was created with 1-methyl-phenyl-1,2,3,6-tetrahydropyridine (MPTP). C57BL/6 breed male mice were randomly divided into six groups: control, K252a, MPTP, MPTP + K252a, MPTP + NaHS, and MPTP + NaHS + K252a. TrkB receptor antagonist K252a and sodium hydrosulfide (NaHS) as a H2S donor were administered intraperitoneally. An increase was observed in the motor behavior tests in MPTP group, but NaHS treatment shortened the time spent on the balance beam and pole tests. It was also noticed that the BDNF-pathway played a role in the shortening of this period. Mice that received NaHS were found to have less MPTP-induced cellular damage. A positive effect of BDNF was also detected in the protection of these neurons. BDNF levels in the SN were significantly increased in MPTP group, compared to control group. Tissue CBS levels decreased in the groups that received K252a, compared to MPTP group. The findings of the present study display that the BDNF-TrkB pathway partially plays a role in the protective effect of H2S in the experimental mouse model of PD. This effect is probably due to changes in intracellular signaling pathways, rather than TrkB receptor expression.