Intracerebral hemorrhage is reported to induce the generation of reactive oxygen species and oxidative DNA damage in the brain. We aimed to examine whether our designed redox polymer nanoparticle could reduce intracerebral hemorrhage induced by 1-MHz focused ultrasound sonication coupled with microbubble treatment. Contrast-enhanced ultrasound imaging, frozen section, brain edema, neurologic deficit, the number of morphologically normal neurons, DNA oxidization and superoxide anion generation were used to investigate the neuroprotective effect of redox polymer nanoparticles. We confirmed that the 1-MHz focused ultrasound coupled with microbubble produced intracerebral hemorrhage and showed that the redox polymer nanoparticle ameliorates intracerebral hemorrhage-induced brain edema, neurological deficit and oxidative damage. These results suggest that redox polymer nanoparticle is a potential therapeutic agent for intracerebral hemorrhage induced by focused ultrasound.

This study aimed to investigate the effect of astaxanthin (ASX) extracted and ASX powder from shrimp (Litopenaeus vannamei) shells on Wistar rats with Alzheimer’s disease, induced by amyloid-β (1-42) peptides. In this task, the rats were divided into eight groups: (1) Control, (2) sham operate, (3) negative control (vehicle) + Aβ_1-42, (4) ASX extract+Aβ_1-42, (5) commercial ASX + Aβ_1-42, (6) ASX powder + Aβ_1-42, (7) blank powder + Aβ_1-42, and (8) vitamin E + Aβ_1-42. All treatments were orally administrated for 30 days. At 14- and 29-days post injection, animals were observed in behavioral tests. On the 31st day, animals were sacrificed; the hippocampus and cortex were collected. Those two brain areas were then homogenized and stored for biochemical and histological analysis. The results showed that the Aβ_1-42 infused group significantly reduced cognitive ability and increased memory loss, as assessed by the Morris water maze test, novel object recognition test, and novel object location test. Moreover, the Aβ_1-42 infused group exhibited a deterioration of oxidative markers, including glutathione peroxidase enzymes (GPx), lipid peroxidation (MDA), products of protein oxidation, and superoxide anion in the cortex and the hippocampus. Meanwhile, ASX powder (10 mg/kg body weight) showed a significant reduction in cognitive and memory impairments and oxidative stress which is greater than ASX extract in the same dose of compound or vitamin E (100 mg/kg body weight). Our study indicates the beneficial properties of ASX in alleviation of cognitive functions and reducing neurodegeneration in Wistar rats induced by amyloid-β (1-42) peptides.

Patients regularly taking non-steroidal anti-inflammatory drugs (NSAIDs) such as indomethacin (IND) have a risk of small intestinal injuries. In this study, we have developed an oral nanotherapeutics by using a redox nanoparticle (RNP(O)), which is prepared by self-assembly of an amphiphilic block copolymer that possesses nitroxide radicals as side chains of hydrophobic segment via ether linkage, to reduce inflammation in mice with IND-induced small intestinal injury. The localization and accumulation of RNP(O) in the small intestine were determined using fluorescent-labeled RNP(O) and electron spin resonance. After oral administration, the accumulation of RNP(O) in both the jejunum and ileum tissues was about 40 times higher than those of low-molecular-weight nitroxide radical compounds, and RNP(O) was not absorbed into the bloodstream via the mesentery, thereby avoiding the adverse effects of nitroxide radicals in the entire body. RNP(O) remarkably suppressed inflammatory mediators such as myeloperoxidase, superoxide anion, and malondialdehyde in the small intestines of IND-treated mice. Compared to low-molecular-weight nitroxide radical compounds, RNP(O) also significantly increased the survival rate of mice treated daily with IND. On the basis of these results, RNP(O) is promising as a nanotherapeutics for treatment of inflammation in the small intestine of patients receiving NSAIDs.