Zinc supplementation ameliorates sorafenib-induced cognitive impairment through ROS/JNK signaling pathway.

Sorafenib, a multiple kinase inhibitor, is widely used in cancer patients. Recently, clinical studies highlighted the relationship between cognitive deficits and sorafenib exposure. Zinc abundant in the body has been reported to exert neuroprotective activities. However, the effects of zinc supplementation on sorafenib-induced cognitive impairment are still unknown. In the current study, we verified that mice challenged with sorafenib displayed characteristic features of cognitive impairment. However, zinc treatment effectively improved these changes. Histopathological staining also showed that zinc significantly alleviated hippocampal microstructural and ultrastructural damages induced by sorafenib. Meanwhile, zinc significantly reduced sorafenib-induced ROS production and neuronal cells apoptosis in vivo and vitro. Additionally, we also investigated whether zinc protected against sorafenib-induced neuronal cells apoptosis via ROS/JNK pathway through treating SH-SY5Y cells with the NAC or the specific JNK activator anisomycin. The results indicated that NAC performed the same protective effects as zinc in sorafenib-challenged SH-SY5Y cells and activation of JNK by anisomycin partly abolished the protective effects of zinc. Collectively, the present study suggested that inhibition of oxidative stress and the JNK pathway might contribute to the protective effects of zinc against sorafenib-caused cognitive impairment in vivo and vitro.

Effects of ultra-high pressure treatment on structure and bioactivity of polysaccharides from large leaf yellow tea.

In this study, the changes of structure and bioactivity of polysaccharides from large leaf yellow tea (LYTP) were investigated under ultra-high pressure (UHP). Native yellow tea polysaccharide were treatmented with ultra-high pressure (200, 400 and 600 MPa) for 5 min to yield yellow tea polysaccharide including 200 MPa-LYTP, 400 MPa-LYTP and 600 MPa-LYTP. It was found that the monosaccharide composition of LYTP changed significantly after the ultra-high pressure treatment. The molecular weight (Mw) of 200 MPa-LYTP (from 563.6 to 11.7 kDa), 400 MPa-LYTP (from 372.2 to 11.8 kDa) and 600 MPa-LYTP (from 344 to 11.6 kDa) sharply decreased upon ultra-high pressure treatment compared with LYTP (771.5 kDa), coincidentally particle size was also significantly reduced for 200 MPa-LYTP (23.2 %), 400 MPa-LYTP (40.2 %) and 600 MPa-LYTP (25.9 %). The results of the scanning electron microscope showed that ultra-high pressure also changed the surface and spatial morphology of LYTP. LYTP after ultra-high pressure treatment (UHP-LYTP) could further ameliorate alcohol-induced liver injury in mice. In addition, UHP treatment can more efficiently remove protein than the Sevages method. With the gradual removal of protein, its hepatoprotective effect increased. These findings demonstrated that UHP treatment could change the primary structure and spatial structure of LYTP, increase the content of acidic polysaccharides, and improve its bioactivity.

Huaier extract restrains pancreatic cancer by suppressing Wnt/ß-catenin pathway.

Pancreatic cancer is a lethal disease, and new treatments need to be explored. Huaier extract is a traditional Chinese medicine that has been found to exert antitumor properties in some cancers. However, the role of Huaier extract in pancreatic cancer has not been examined. In this study, we found that the proliferation, migration, invasion and EMT (epithelial-mesenchymal transition) of pancreatic cancer cells were suppressed by treatment with Huaier extract and that apoptosis increased. We also observed that expression of ß-catenin was inhibited by Huaier extract. Furthermore, an animal study showed that Huaier extract slowed tumor growth in pancreatic cancer. Our results reveal that Huaier extract suppresses pancreatic cancer by inhibiting Wnt/ß-catenin pathway both in vitro and in vivo.

Preventive Effects of the Intestine Function Recovery Decoction, a Traditional Chinese Medicine, on Postoperative Intra-Abdominal Adhesion Formation in a Rat Model.

The intestine function recovery decoction (IFRD) is a traditional Chinese medicine that has been used for the treatment of adhesive intestinal obstruction. In this study, the preventative effects and probable mechanism of the IFRD were investigated in a rat model. We randomly assigned rats to five groups: normal, model, control, low dose IFRD, and high dose IFRD. In the animal model, the caecum wall and parietal peritoneum were abraded to induce intra-abdominal adhesion formation. Seven days after surgery, adhesion scores were assessed using a visual scoring system, and histopathological samples were examined. The levels of serum interleukin-6 (IL-6) and transforming growth factor beta-1 (TGF-ß1) were analysed by an enzyme-linked immunosorbent assay (ELISA). The results showed that a high dose of IFRD reduced the grade of intra-abdominal adhesion in rats. Furthermore, the grades of inflammation, fibrosis, and neovascularization in the high dose IFRD group were significantly lower than those in the control group. The results indicate that the IFRD can prevent intra-abdominal adhesion formation in a rat model. These data suggest that the IFRD may be an effective antiadhesion agent.