Controllable silicon nanostructures featuring stable fluorescence and intrinsic in vitro and in vivo anti-cancer activity.

In this manuscript, we demonstrate that the in situ growth of fluorescent silicon (Si) nanomaterials is stimulated when organosilicane molecules interact with different green teas, producing multifunctional Si nanomaterials with controllable zero- (e.g., nanoparticles), two- (e.g., nanosheets), and three- (e.g., nanospheres) dimensional nanostructures. Such green tea-originated Si nanomaterials (GTSN) exhibit strong fluorescence (quantum yield: ∼19-30%) coupled with ultrahigh photostability, as well as intrinsic anti-cancer activity with high specificity (e.g., the GTSN can accurately kill various cancer cells, rather than normal cells). Taking advantage of these unique merits, we further performed systematic in vitro and in vivo experiments to interrogate the mechanism of the green tea- and GTSN-related cancer prevention. Typically, we found that the GTSN entered the cell nuclei and induced cell apoptosis/death of cancer cells. The prepared GTSN were observed in vivo to accumulate in the tumour tissues after 14-d post-injection, leading to an efficient inhibition of tumour growth. Our results open new avenues for designing novel multifunctional and side-effect-free Si nanomaterials with controllable structures.

Multifunctional Silicon-Carbon Nanohybrids Simultaneously Featuring Bright Fluorescence, High Antibacterial and Wound Healing Activity.

In this work, a class of multifunctional silicon-carbon nanohybrids (designated as SiCNs), which simultaneously possess aqueous dispersibility, bright fluorescence (photoluminescence quantum yield [PLQY]: ≈28%), as well as high antibacterial and wound healing activity, is presented. Taking advantage of these unique merits, cell distribution and pharmacological behavior of the SiCNs is first investigated through tracking their strong and stable fluorescence. The high bacteria inhibition ability (≈82.9% killing rate toward S. aureus) and hemostatic effects (shorten the bleeding time from ≈60 to ≈15 s) of the resultant SiCNs are then demonstrated. Moreover, the wound closure promotion activity (10% lead in wound contraction) is systematically demonstrated in vivo, which is especially suitable for wound healing applications. The results suggest the SiCNs as a new kind of high-performance multifunctional nanoagents suitable for various biological and biomedical utilizations.

A novel IgG1 monoclonal antibody against xanthine oxidase alleviates inflammation induced by potassium oxonate in mice.

Xanthine oxidase (XOD) is a key enzyme that catalyzes xanthine to uric acid. Most of the urate-lowering medicines targeting XOD have a limited effect on alleviating inflammation in spite of significant effects on decreasing serum uric acid level. In this study, we produced and characterized a novel monoclonal antibody (Anti-XOD mAb) using hybridoma technology based on a novel peptide OI5P-1(O-IA2(5)-P2-1),which containing a B-cell epitope of XOD and a novel Th2 built-in adjuvant I5P-1(IA2(5)-P2-1). Results of western blotting and cross-reactivity assay indicated that the mAb binds specifically to XOD and the affinity was 2.523×1010L/mol. The mAb reduced serum uric acid level and hepatic xanthine oxidase activity in potassium oxonate induced mice. A decreased methane dicarboxylic aldehyde level and an improved superoxide dismutase level in mAb treated mice indicated anti-lipid peroxidation effects of the mAb. Moreover, the mAb showed a significant immunomodulatory effect which could shift Th1/Th2 balance to Th2-dominant immunity. The mAb treatment alleviates inflammation induced by potassium oxonate, superior to the small molecule allopurinol treatment. For the first time, these results showed that the anti-XOD mAb may serve as a promising therapeutic approach for inflammatory response related to uric acid.

Aprotinin combined with nitric oxide and prostaglandin E1 protects the canine kidney from cardiopulmonary bypass-induced injury.

OBJECTIVE: Aprotinin is frequently used to reduce blood loss during cardiac surgery; however, it also causes renal injury. Since aprotinin reduces nitric oxide (NO) and prostaglandin I(2) (PGI(2)), and both cause vasodilation and inhibit activation of neutrophils and platelets, their reduction may be responsible for the injury. This study was to determine whether the combination of aprotinin with NO and prostaglandin E(1) (PGE(1), an analogue of PGI(2)) can attenuate renal injury associated with aprotinin during cardiopulmonary bypass (CPB). METHODS: Thirty mongrel dogs were equally divided into five groups, with each group receiving CPB and aprotinin, NO, PGE(1), a combination of the three or no treatment (control). Serum creatinine and creatinine clearance were determined. To elucidate the mechanism, neutrophil, platelet and thrombin activations were also assessed. RESULTS: After CPB, serum creatinine increased and creatinine clearance decreased in all dogs. These changes were similar among the NO, PGE(1), aprotinin and control groups, but were significantly smaller in the combination group. Similarly, myeloperoxidase activities in tissues, CD11b expression, plasma elastase, prothrombin fragment (PTF) 1+2 and platelet activation factor were lower, whereas neutrophil and platelet counts were higher in the combination group than in the other groups (P<0.05). CONCLUSIONS: Aprotinin combined with NO and PGE(1) produced synergistic protective effects and improved renal function, due partly to inhibition of platelet and neutrophil activation and suppression of thrombin formation.