Dispersibility of TiO2 Nanoparticles in Less Polar Solvents: Role of Ligand Tail Structures.

Nanoparticles (NPs) are inherently prone to aggregation and loss of their size-derived properties, thus it is essential to enhance their dispersibility for applications. In less polar solvents, organic ligands containing oleyl groups are known as good dispersants due to their inefficient shell packing and inhibition of chain-chain crystallization as well as interdigitation between adjacent NPs. However, reagents with oleyl structures, such as oleic acid and oleylamine, can contain trans double bonds and saturated impurities, which might affect the chemical and/or physical properties of the NPs. Nevertheless, the effect of slight differences in surface ligand structure, including isomers, on the dispersibility of NPs has been little studied. We have synthesized five phosphonic acid ligands to investigate the structure-dispersibility relationship in detail. Dynamic light scattering and visible light transmittance revealed that not only regio- but also the stereochemistries of the C=C double bond in the ligand molecule, as well as the choice of solvent, are key factors in enhancing dispersibility.

Investigation of the Oral Retention of Tea Catechins in Humans: An Exploratory Interventional Study.

Green tea catechin ingestion or gargling exhibit anti-viral activity against upper respiratory infection. We hypothesized that retention in the oral cavity could improve the anti-viral effects of catechins. The present study investigated the oral retention of catechins in humans and the effect of catechin beverage viscosity on oral retention. Two intervention studies with different test beverages, beverage-C (40 mL, containing 73.4 mg of catechins) and beverage-XT (40 mL, beverage-C containing 100 mg xanthan gum) were conducted in 20 healthy volunteers (mean age 38.7 years). Catechin concentrations were measured in buccal mucosa samples collected at 10 min, 40 min, and 60 min after ingesting test beverages, and the catechin variability of the tissue after intake was compared between test beverages. As a result, the mean (SEM) concentrations of EGCG were 99.9 (27.2), 58.2 (16.6), and 22.3 (5.7) ng/mg-mucosa at 10, 40, and 60 min, respectively, after ingestion of beverage-XT. Similarly, the catechin concentrations were 86.1 (20.3), 32.2 (5.3), and 27.8 (5.9) ng/mg-mucosa after ingestion of beverage-C. The total retention volume over 60 min tended to be slightly higher after ingestion of beverage-XT, though the difference was not statistically significant. Additional studies are needed to confirm the effect of xanthan gum on improving oral retention of catechins.

Effect of edaravone against cisplatin-induced chronic renal injury.

Cisplatin has been widely used as an anticancer agent for a wide range of tumors, but it had nephrotoxicity that was mainly caused by oxidative stress. Edaravone, a free radical scavenger, has reportedly been validated to have a protective effect against renal injury induced by reactive oxygen species. However, most of these reports are against AKI, and few studies have examined the effect of chronic renal injury. In this study, we investigate the effect of edaravone on cisplatin nephropathy in the chronic phase. Twenty-five male Wistar rats were divided into five groups: control, cisplatin, cisplatin + edaravone 1 mg kg-1, cisplatin + edaravone 10 mg kg-1, and cisplatin + edaravone 100 mg kg-1. Edaravone was administrated intraperitoneally every other day for 5 weeks, starting 1 week before cisplatin administration (6 mg kg-1, i.p.). As a result, proximal tubule injury, interstitial fibrosis, and mononuclear cell infiltration were ameliorated histologically in the group of rats treated with high edaravone dose. In the cisplatin group, the number of α-SMA-, CD68-, and CD3-positive cells increased markedly compared with the Control group, but these numbers were significantly decreased by higher doses of co-administered edaravone. While there was no clear mRNA expression variation in antioxidant enzymes, the apoptosis-promoting factors, caspase8, were markedly reduced in the high-dose edaravone co-administration group compared with the cisplatin group. In conclusion, our results suggested that cisplatin-induced renal injury in the chronic phase was ameliorated by edaravone.

Dimethyl fumarate ameliorates cisplatin-induced renal tubulointerstitial lesions.

Dimethyl fumarate (DMF) has an antioxidant effect by activating the nuclear factor erythroid 2-related transcription factor 2 (Nrf2). Cisplatin (CIS) has nephrotoxicity as a frequently associated side effect that is mainly mediated by oxidative stress. In this study, we investigated whether the DMF-mediated antioxidative mechanism activated by Nrf2 can ameliorate CIS-induced renal tubulointerstitial lesions in rats. In Experiments 1 and 2, 25 five-week-old male Wistar rats were divided into five groups: control, CIS, and 3 CIS+DMF groups (300, 1,500, and 7,500 ppm in Experiment 1; 2,000, 4,000, and 6,000 ppm in Experiment 2). Rats were fed their respective DMF-containing diet for 5 weeks. CIS was injected 1 week after starting DMF administration, and the same volume of saline was injected into the control group. CIS-induced severe tubular injury, such as necrosis and degeneration in the outer segment of the outer medulla, was inhibited in the 7,500 ppm DMF group and ameliorated in all DMF groups in Experiment 2. Increased interstitial mononuclear cell infiltration and increased Sirius red-positive areas were also observed in CIS-administered groups, and these increases tended to be dose-dependently inhibited by DMF co-administration in Experiments 1 and 2. The numbers of α-smooth muscle actin (SMA)-positive myofibroblasts, CD68-positive macrophages, and CD3-positive lymphocytes observed in the peritubular area also increased with CIS administration, and these increases were dose-dependently inhibited by DMF co-administration. Moreover, renal cortical mRNA expression of Nrf2-related genes such as NQO1 increased in DMF groups. This investigation showed that DMF ameliorates CIS-induced renal tubular injury via NQO1-mediated antioxidant mechanisms and reduces the consequent tubulointerstitial fibrosis.