Jun Yi

BACKGROUND: Snakebites remain a major life-threatening event worldwide. It is still difficult to make a positive identification of snake species by clinicians in both Western medicine and Chinese medicine. The main reason for this is a shortage of diagnostic biomarkers and lack of knowledge about pathways of venom-induced toxicity. In traditional Chinese medicine, snakebites are considered to be treated with wind, fire, and wind-fire toxin, but additional studies are required. METHODS: - and wind-fire toxin - four cases of bites by vipers and three bites by cobras. Serum protein quantification was performed using LC-MS/MS. Differential abundance proteins (DAPs) were identified from comparison of snakebites of each snake species and healthy controls. The protein interaction network was constructed using STITCH database. RESULTS: Principal component analysis and hierarchical clustering of 474 unique proteins exhibited protein expression profiles of wind-fire toxins that are distinct from that of fire toxins. Ninety-three DAPs were identified in each snakebite subgroup as compared with healthy control, of which 38 proteins were found to have significantly different expression levels and 55 proteins displayed no expression in one subgroup, by subgroup comparison. GO analysis revealed that the DAPs participated in bicarbonate/oxygen transport and hydrogen peroxide catabolic process, and affected carbon-oxygen lyase activity and heme binding. Thirty DAPs directly or indirectly acted on hydrogen peroxide in the interaction network of proteins and drug compounds. The network was clustered into four groups: lipid metabolism and transport; IGF-mediated growth; oxygen transport; and innate immunity. CONCLUSIONS: Our results show that the pathways of snake venom-induced toxicity may form a protein network of antioxidant defense by regulating oxidative stress through interaction with hydrogen peroxide.

In this study, we aimed to investigate the role of miR-877-5p in the malignant phenotypes of prostate cancer (PCa) cells and its underlying mechanism. RT-qPCR analysis was performed to examine the expression of miR-877-5p and sperm-specific antigen 2 (SSFA2) in PCa tissues and cells. Cell counting kit-8 (CCK-8) assay, 5-ethynyl-20-deoxyuridine (EdU) assay, flow cytometry, wound-healing assay, and Transwell invasion assay were performed to determine the functional roles of miR-877-5p in PCa cells. The association of miR-877-5p with SSFA2 was determined by luciferase reporter and RNA pull-down assays. In this study, we found that the expression level of miR-877-5p was decreased in PCa tissues and cells. Functionally, overexpression of miR-877-5p exerted tumor suppressor properties in PCa cells. Mechanistically, SSFA2 was identified as a target gene of miR-877-5p, while overexpression of SSFA2 could abrogate the anti-tumor effects of miR-877-5p in PCa cells. These findings demonstrated that miR-877-5p/SSFA2 axis functioned as a potential target for PCa treatment.

BACKGROUND: Chronic non-bacterial prostatitis (CNBP) accounts for more than 90 % of clinical prostatitis cases, and there is no specific and effective treatment for CNBP. The regulatory role of Jiedu Huoxue decoction (JDHXD)in CNBP remains unclear. We investigated if JDHXD could improve CNBP METHODS: The animal model of CNBP was established by carrageenan injection with 1 % carrageenan (50 μL). The prostate index, epithelial thickness, lumen area, and pain response time were investigated. The apoptosis levels were measured with TUNEL staining and flow cytometry, respectively. Inflammatory factors in the serum were measured with ELISA method. RESULTS: Treatment with JDHXD significantly improve prostate tissues injury in CNBP rats. Some parameters, such as prostate index, and pain response time, reflecting the prostate function were improved by JDHXD. Inhibition of apoptosis, reactive oxygen species (ROS), and inflammatory response were achieved by JDHXD in vivo. JDHXD markedly suppressed the TGF-β/SMAD signaling pathway, and activation of TGF-β/SMAD signaling pathway could reverse the improvement of CNBP injury by JDHXD. The anti-inflammatory, anti-oxidative and anti-apoptotic effects of JDHXD were proved. CONCLUSION: JDHXD might improve CNBP injury through suppressing inflammation response, ROS, and apoptosis by targeting TGF-β/SMAD signaling pathway. This research might provide a new thought for the prevention and treatment of CNBP through inhibiting TGF-β/SMAD signaling pathway.

CONTEXT: The underlying mechanisms of Jiedu Huoxue decoction (JDHXD) in treating chronic prostatitis have not been fully explored. OBJECTIVE: This study investigates the miRNAs as potential biomarkers and the effect of JDHXD on the rat model of experimental nonbacterial prostatitis. MATERIALS AND METHODS: Fifty-four Sprague-Dawley male rats were randomly divided into normal control, model, JDHXD low dose (0.5 g/kg/day), medium dose (1 g/kg/day), high dose (2 g/kg/day) and western medicine (cernilton 0.094 g/kg/day) groups, and intragastrically administered once daily for 30 days. The control and model (upon successful establishment) groups received distilled water. Differential expression of miRNAs was analysed with high-throughput miRNA sequencing and validated with qRT-PCR and Northern blot. Prediction of specific target genes and functional enrichment analysis were performed with bioinformatics. RESULTS: > 0.05). DISCUSSION AND CONCLUSIONS: Future studies may explore the contributions of the active components in JDHXD. The study design is generalisable. The effect can be repeatedly verified in clinical trials.