ABSTRACT
Cisplatin， as one of the commonly used broad-spectrum anti-tumor drugs in clinical practice， is used to treat testicular cancer， ovarian cancer， head and neck cancer， bladder cancer， lung cancer， cervical cancer and other solid cancers. It has obvious curative effect but strong toxic and side effect， and is easy to cause great damage to the body. The toxic reaction may involve serious toxic damages to different organs， and induce nephrotoxicity， hepatotoxicity， ototoxicity， cardiotoxicity， neurotoxicity and other toxicity. Animal experiments have shown that the toxic damage induced by cisplatin is the result of many factors in a time-and dose-dependent manner. In the course of clinical use， the therapeutic dose of cisplatin is also greatly limited due to toxic damage， which seriously affects the quality of life in patients. Therefore， it is the main research direction to find a suitable treatment plan or to use drugs in combination with cisplatin to reduce toxicity and increase efficiency. With the increasing clinical participation of traditional Chinese medicine（TCM）， TCM has shown its unique advantages in treating diseases， and can effectively reduce the cisplatin chemotherapy-induced toxic reaction by improving the oxidative stress state of the body， inhibiting normal apoptosis and inflammatory injury， activating autophagy， regulating the abnormal expression of drug transporters， etc. In this paper， the mechanism of cisplatin-induced toxic damage to various organs and the mechanism of TCM in prevention and treatment of cisplatin-induced toxic damage were summarized in detail， including the dose and mechanism of cisplatin-induced toxic damage to different organs， the effective treatment dose， combined medication mode and prevention and treatment mechanism of combined application of TCM and cisplatin， in order to provide a basis for rational application and clinical medication of TCM combined with chemotherapy drugs such as cisplatin.
ABSTRACT
<p><b>BACKGROUND</b>Glucagon-like peptide-1 (GLP-1) reduces fatty acid-induced beta-cell lipotoxicity in diabetes; however, the explicit mechanisms underlying this process are not fully understood. This study was designed to investigate the involvement of microRNA, which regulates gene expression by the sequence-specific inhibition of mRNA transcription in the GLP-1 mediation of beta-cell function.</p><p><b>METHODS</b>The cell viability and apoptosis were determined using an methyl thiazoleterazolium (MTT) assay and flow cytometry. The expression of genes involved in beta-cell function, including microRNA-34a and sirtuin 1, were investigated using real-time PCR. The underlying mechanisms of microRNA-34a were further explored using cell-transfection assays.</p><p><b>RESULTS</b>A 24-hours incubation of INS-1 cells with palmitate significantly decreased cell viability, increased cell apoptosis and led to the activation of microRNA-34a and the suppression of sirtuin 1. A co-incubation with GLP-1 protected the cells against palmitate-induced toxicity in association with a reduction in palmitate-induced activation of microRNA-34a. Furthermore, palmitate-induced apoptosis was significantly increased in cells that were infected with microRNA-34a mimics and decreased in cells that were infected with microRNA-34a inhibitors.</p><p><b>CONCLUSION</b>MicroRNA-34a is involved in the mechanism of GLP-1 on the modulation of beta-cell growth and survival.</p>