Tailoring the surface properties of poly(dimethylsiloxane) (PDMS) is essential for the advancement of its applications. However, the modification process is usually complicated and limited due to the chemical inertness of the surfaces of PDMS. Here, we report for the first time, a facile and versatile method for the functional surface modification of PDMS via visible light-induced grafting polymerization at room temperature. This modification is readily achieved in two steps: (1) covalently integrating alkyl bromine into the PDMS networks using a simple mixing procedure and (2) visible light-induced surface grafting polymerization using Mn2(CO)10. We have demonstrated that the PDMS surface can be functionalized with a wide variety of polymers via covalent grafting, such as poly(trifluoroethyl methacrylate) (PTFEMA), poly(N-isopropylacrylamide) (PNIPAAm), poly(acrylic acid) (PAA) and poly(vinyl acetate) (PVAc). As an example, after the grafted PVAc was transformed into its hydrophilic analogue poly(vinyl alcohol) (PVA), anti-biofouling functionalization of PDMS was obtained. The anti-biofouling properties of the functionalized PDMS were demonstrated using cell adhesion and bacterial adhesion tests. Moreover, the grafting kinetics of PVAc showed that this process was fast and efficient.
Reactive oxygen species (ROS)-associated anticancer approaches usually suffer from two limitations, i.e., insufficient ROS level and short ROS half-life. Nevertheless, no report has synchronously addressed both concerns yet. Herein, a multichannel actions-enabled nanotherapeutic platform using hollow manganese dioxide (H-MnO 2 ) carriers to load chlorin e6 (Ce6) sonosensitizer and CO donor (e.g., Mn 2 (CO) 10 ) has been constructed to maximumly elevate ROS level and trigger cascade catalysis to produce CO. Therein, intratumoral H 2 O 2 and ultrasound as endogenous and exogeneous triggers stimulate H-MnO 2 and Ce6 to produce •OH and 1 O 2 , respectively. The further cascade reaction between ROS and Mn 2 (CO) 10 proceeds to release CO, converting short-lived ROS into long-lived CO. Contributed by them, such a maximumly-elevated ROS accumulation and long-lived CO release successfully suppresses the progression, recurrence and metastasis of lung cancer with a prolonged survival rate. More significantly, proteomic and genomic investigations uncover that the CO-induced activation of AKT signaling pathway, NRF-2 phosphorylation and HMOX-1 overexpression induce mitochondrial dysfunction to boost anti-tumor consequences. Thus, this cascade catalysis strategy can behave as a general means to enrich ROS and trigger CO release against refractory cancers. Graphic Abstract
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