Low-Field Actuating Magnetic Elastomer Membranes Characterized using Fibre-Optic Interferometry.

Smart robotic devices remotely powered by magnetic field have emerged as versatile tools for wide biomedical applications. Soft magnetic elastomer (ME) composite membranes with high flexibility and responsiveness are frequently incorporated to enable local actuation for wireless sensing or cargo delivery. However, the fabrication of thin ME membranes with good control in geometry and uniformity remains challenging, as well as the optimization of their actuating performances under low fields (milli-Tesla). In this work, the development of ME membranes comprising of low-cost magnetic powder and highly soft elastomer through a simple template-assisted doctor blading approach, is reported. The fabricated ME membranes are controllable in size (up to centimetre-scale), thickness (tens of microns) and high particle loading (up to 70 wt.%). Conflicting trade-off effects of particle concentration upon magnetic responsiveness and mechanical stiffness are investigated and found to be balanced off as it exceeds 60 wt.%. A highly sensitive fibre-optic interferometric sensing system and a customized fibre-ferrule-membrane probe are first proposed to enable dynamic actuation and real-time displacement characterization. Free-standing ME membranes are magnetically excited under low field down to 2 mT, and optically monitored with nanometer accuracy. The fast and consistent responses of ME membranes showcase their promising biomedical applications in nanoscale actuation and sensing.

Naringenin Ameliorates Doxorubicin Toxicity and Hypoxic Condition in Dalton's Lymphoma Ascites Tumor Mouse Model: Evidence from Electron Paramagnetic Resonance Imaging.

Doxorubicin (DOX) is a well-known cytotoxic agent used extensively as a chemotherapeutic drug to eradicate a wide variety of human cancers. Reactive oxygen species (ROS)-mediated oxidative stress during DOX treatment can induce cardiac, renal, and hepatic toxicities, which can constrain its use as a potential cytotoxic agent. The present work investigates the antioxidant potential of naringenin (NAR) against DOXinduced toxicities of a Dalton's lymphoma ascites (DLA) tumor-bearing mouse model. Mice were randomized into four groups: a negative control, positive control, DOX (2.5 mg/kg) treated, and DOX (2.5 mg/kg) + NAR (50 mg/kg/d) treated. DOX administration significantly altered the levels of functional markers in blood and antioxidant enzymes in kidney, heart, lung, liver, spleen, and tumor tissues. These changes in antioxidant enzymes and successive lipid peroxidation were prevented by NAR supplementation, resulting in decreases in the risk of toxicity due to DOX therapy. Histopathology results and electron paramagnetic resonance imaging (EPRI) of the tumor microenvironment confirmed this evidence. Using EPRI, pharmacokinetics of the nitroxide, 3-carbamoyl-2,2,5,5-tetramethylpyrrolidine-1-oxyl (3-CP) was monitored intratumorally before and after chemotherapy. EPRI of the DOX + NAR-treated mouse model showed reduced tumor size with significant modification of the hypoxic condition inside the tumor microenvironment. Consequently, these findings suggest that NAR treatment significantly reduces DOX-induced toxicity and the hypoxic condition in a DLA tumor-bearing mouse model.

Protective role of naringenin against doxorubicin-induced cardiotoxicity in a rat model: histopathology and mRNA expression profile studies.

Doxorubicin (DOX) is one of the most effective and widely used chemotherapeutic agents. Its efficacy has been proven in various malignancies alone and combined with other cytocidal agents. However, the clinical usefulness of DOX is restricted by the risk of developing congestive heart failure. Formation of free radicals and oxidative stress during DOX treatment may result in adverse side effects. Naringenin (NAR) is one of the potential bioflavonoids with excellent antioxidant properties and free-radical scavenging capability. This study was designed to evaluate whether NAR exerts a protective role against DOX-induced cardiotoxicity in rats. Male Wistar rats were administered DOX (3 mg/kg) intravenously for 10 consecutive weeks along with oral treatment with NAR (50 mg/kg/day). DOX-induced cardiac toxicity was characterized by the marked biochemical alterations of lactic acid dehydrogenase (LDH), troponin T, malondialdehyde (MDA), reduced cardiac enzymatic activities (SOD, GPx, CAT) and histopathological observations. Administration of NAR to DOX-challenged rats ameliorated alterations in biochemical markers. Indeed, DOX increased the mRNA expression levels of TGF-ß1, TNF-α, IL-6, and IL-10 compared with the control group. However, cotreatment with NAR attenuated the mRNA expression levels of these inflammatory markers and improved histological cardiac damage and cardiac functions. Thus, supplementation of NAR may be beneficial in reducing DOX toxicity.