HP-1 inhibits the progression of ccRCC and enhances sunitinib therapeutic effects by suppressing EMT.

Trametes robiniophila Murr (Huaier) has been used for many years as an adjuvant treatment for tumors. Sunitinib is the first-line therapy for end-stage renal cancer, but its side effects and drug resistance limit its clinical application. Cell counting kit- 8 (CCK-8), colony formation, scratch, and Transwell assays showed that Huaier polysaccharide (HP-1) reduced tumor progression. Its combination with sunitinib elicited stronger antitumor effects, including induction of apoptosis and cycle arrest. HP-1-induced effects depended on CIP2A downregulation and suppression of the EMT process. Moreover, qPCR and western blotting experiments showed that CIP2A downregulation was particularly pronounced after treatment with the combination therapy and was associated with EMT suppression. In addition, the HP-1/sunitinib combination inhibited the PI3K/Akt/VEGFR pathway, reducing the expression of pathway-related proteins. The HP-1-induced enhancement of sunitinib effects on tumor growth were also observed in vivo in a xenograft mouse model. Overall, these results indicated that HP-1 exerted antitumor effects against clear cell renal cell carcinoma (ccRCC) and enhanced the therapeutic efficacy of sunitinib.

A polysaccharide from Huaier ameliorates cisplatin nephrotoxicity by decreasing oxidative stress and apoptosis via PI3K/AKT signaling.

Cisplatin (CP), a common chemotherapy drug used in treatment of malignant tumors. Due to various side effects such as nephrotoxicity (kidney damage), it's efficiency and therapeutic application are limited. This study focuses on finding a suitable drug that would attenuate the side effects like kidney damage, caused by CP. Huaier polysaccharide (HP-1), an extraction of Trametes robiniophila Murr, with a molecular weight of 3 × 104 Da. Previous studies have shown that HP-1, exhibits anti-tumor potential and immunomodulatory effects. We hypothesized that HP-1 has the effect of attenuating the nephrotoxicity caused by CP chemotherapy and protecting renal function. Through our experiments, we observed that HP-1 can attenuate the level of oxidative stress, inflammation and mitochondrial dysfunction, thereby reducing kidney damage. In vitro, we observed that HP-1 significantly inhibits CP-induced renal tubular cell apoptosis and cell cycle arrest. In addition, HP-1 also affects the expression level of the protein by regulating the PI3K/Akt/mTOR signaling pathway and thus attenuates the side effects induced by cisplatin. Therefore, HP-1 may be a potential drug for preventing CP-induced renal damage.

The selective catalytic reduction of NO over Ce0.3TiOx-supported metal oxide catalysts.

A Ce0.3TiOx oxide carrier was synthesized via a sol-gel process, and Ce0.3TiOx supported metal (M=Cd, Mn, Fe, W, Mo) oxide catalysts were prepared by the method of incipient-wetness impregnation. The catalysts were characterized by means of X-ray diffraction (XRD), Brunauer-Emmett-Teller (BET) analysis, scanning electron microscopy (SEM), transmission electron microscopy (TEM), Fourier transform infrared (FT-IR) spectroscopy, UV-Vis diffuse reflectance spectroscopy (UV-Vis DRS), and Temperature-programmed reduction with H2 (H2-TPR). The catalytic activities for de-NOx were evaluated by the NH3-SCR reaction. Among all the catalysts tested, the 2wt.% Cd/Ce0.3TiOx catalyst exhibited the best NH3-SCR performance, with a wide temperature window of 250-450°C for NO conversion above 90%. Moreover, the catalyst showed N2 selectivity greater than 99% from 200 to 450°C.