Integrating uniform design and response surface methodology to optimize thiacloprid suspension.

A model 25% suspension concentrate (SC) of thiacloprid was adopted to evaluate an integrative approach of uniform design and response surface methodology. Tersperse2700, PE1601, xanthan gum and veegum were the four experimental factors, and the aqueous separation ratio and viscosity were the two dependent variables. Linear and quadratic polynomial models of stepwise regression and partial least squares were adopted to test the fit of the experimental data. Verification tests revealed satisfactory agreement between the experimental and predicted data. The measured values for the aqueous separation ratio and viscosity were 3.45% and 278.8 mPa·s, respectively, and the relative errors of the predicted values were 9.57% and 2.65%, respectively (prepared under the proposed conditions). Comprehensive benefits could also be obtained by appropriately adjusting the amount of certain adjuvants based on practical requirements. Integrating uniform design and response surface methodology is an effective strategy for optimizing SC formulas.

Phoxim Microcapsules Prepared with Polyurea and Urea-Formaldehyde Resins Differ in Photostability and Insecticidal Activity.

The application of pesticide microcapsules (MCs) in agriculture is becoming more and more popular. In this study, the effects of different wall materials on the stomach toxicity, contact toxicity, length of efficacy, and photolysis characteristics of pesticide microcapsules were investigated. The results showed that microencapsulation reduced the stomach and contact toxicities of phoxim and prolonged the efficacy of this light-sensitive chemical in the greenhouse test. Neither of the degradation curves for microencapsulated phoxim under ultraviolet light fit a first-order model, although the emulsifiable concentrate (EC) degradation curve fit it well. The phoxim-loaded polyurea microcapsules (PUA-MCs) showed significantly increased UV-resistance ability, stomach toxicity, and contact toxicity compared with the phoxim-loaded urea-formaldehyde microcapsules (UF-MCs). These experiments indicated that it is crucial to select the appropriate wall materials for pesticide microcapsules on the basis of application sites and physicochemical properties of pesticide active ingredients.

Nitidine chloride induces apoptosis and inhibits tumor cell proliferation via suppressing ERK signaling pathway in renal cancer.

Nitidine chloride (NC), a natural bioactive alkaloid derived from Zanthoxylum nitidum (Roxb) DC, has been shown to have inhibitory effects on various tumors. However, whether NC could exert anti-cancer activity and the underlying mechanisms have not been elucidated in renal cancer cells. In this study, we demonstrated the growth inhibitory and pro-apoptotic effects of NC on renal cancer cells both in vitro and in vivo. With cell viability and flow cytometric apoptosis assays, we found that NC potently suppressed the growth of 786-O and A498 cells in a time- and dose- dependent manner. Consistently, the xenograft model performed in nude mice exhibited reduced tumor growth with NC treatment. Mechanically, we presented that NC significantly decreased phosphorylation of ERK and Akt, accompanied by up-regulation of P53, Bax, cleavage caspase-3 and cleavage PARP, downregulation of Bcl-2, caspase-3 and PARP. Furthermore, a specific MEK inhibitor, PD98059, could potentiate the pro-apoptotic effects of NC, which indicated that NC might trigger apoptosis in renal cancer cells partly via inhibition of ERK activity. Taken together, our results imply that NC could be developed as a potential anticancer agent to renal cancer and worthy of further studies.

Nitidine chloride inhibits renal cancer cell metastasis via suppressing AKT signaling pathway.

Nitidine Chloride (NC) has been shown to have anti-cancer effects on various tumors. However, whether NC could exert anti-metastasis activity in renal cancer cells and the underlying mechanisms have not been elucidated. In this work, our data demonstrated the anti-metastasis effects of NC on renal cancer cells in vitro. With scratch assay and transwell assays, we found that NC potently suppressed the migration and invasion of 786-O and A498 cells. Mechanistically, we presented that NC significantly decreased phosphorylation of AKT, accompanied by down-regulation of MMP-2 and MMP-9. Furthermore, a specific AKT inhibitor, LY294002, could enhance the anti-metastasis effects of NC, which indicated that NC suppressed metastasis of renal cancer cells partly via inhibition of AKT activity. Taken together, our results imply that NC can be developed as a potential anti-metastasis agent to renal cancer.

Simvastatin inhibits renal cancer cell growth and metastasis via AKT/mTOR, ERK and JAK2/STAT3 pathway.

Renal cell carcinoma (RCC) is the most lethal type of genitourinary cancer due to its occult onset and resistance to chemotherapy and radiation. Recently, accumulating evidence has suggested stains, inhibitors of 3-hydroxy-3-methyl glutaryl coenzyme A (HMG-CoA) reductase, were associated with the risk reduction of cancer. In the present study, we aimed to investigate the potential effects of simvastatin on RCC cells and the underlying mechanisms by which simvastatin exerted its actions. With cell viability, colony formation, and flow cytometric apoptosis assays, we found that simvastatin potently suppressed cell growth of A498 and 786-O cells in a time- and dose- dependent manner. Consistently, the xenograft model performed in nude mice exhibited reduced tumor growth with simvastatin treatment. In addition, the inhibitory effects of simvastatin on migration and invasion were also observed in vitro. Mechanically, we presented that simvastatin could suppress the proliferation and motility of RCC cells via inhibiting the phosphorylation of AKT, mTOR, and ERK in a time- and dose- dependent manner. Further investigation of the underlying mechanism revealed simvastatin could exert the anti-tumor effects by suppressing IL-6-induced phosphorylation of JAK2 and STAT3. In conclusion, these findings suggested that simvastatin-induced apoptosis and its anti-metastasis activity in RCC cells were accompanied by inhibition of AKT/mTOR, ERK, and JAK2/STAT3 pathways, which imply that simvastatin may be a potential therapeutic agent for the treatment of RCC patients.