[Research and application of model fruit fly in prevention and treatment of neuropsychiatric disorders by traditional Chinese medicine and natural compounds: a review].

As an important model animal, fruit fly is characterized by outstanding genetic characteristics, relatively perfect nervous system, rapid reproduction, and low cost. Thus, it has been applied in the research on neuropsychiatric disorders in recent years, showing great potential in life science. The incidence of neuropsychiatric disorders has been on the rise, and the disorders have high disability rate and low case fatality rate. The global drug demand for such diseases is second only to cardiovascular and cerebrovascular diseases. At the moment, the demand of the drugs for the diseases have been rising, and it is an urgent task to develop related drugs. However, the research and development of the drugs are time-intensive and have a high failure rate. A suitable animal model can help shorten the time for drug screening and development, thereby reducing the cost and failure rate. This study reviews the application of fruit flies in several common neuropsychiatric disorders, which is expected to provide new ideas for the research and application of the model animals in traditional Chinese medicine.

Selenium Supplementation Protects Against Lipopolysaccharide-Induced Heart Injury via Sting Pathway in Mice.

Sepsis-induced myocardial dysfunctions are associated with high morbidity and mortality. Selenium, an essential trace element, has been reported to exert anti-inflammation, anti-oxidative stress, and anti-apoptosis. However, the protective effects of selenium on LPS-induced heart injury are still poorly illustrated. Therefore, in the present study, we sought to explore the effects of selenium pretreatment on LPS-induced myocardial injury in mice. We firstly found that selenium pretreatment significantly improved markers of myocardial injury and alleviated LPS-induced myocardial dysfunctions. Moreover, selenium supplementation reduced pro-inflammatory cytokines expression, decreased oxidative stress, and inhibited myocardial apoptosis. In addition, selenium supplementation inactivated the Sting pathway. In conclusion, our study suggests that selenium exerts protective effects on LPS-induced myocardial injury, and the underlying molecular mechanism may be related to the inactivation of Sting pathway, implying a potential therapy for sepsis-induced myocardial dysfunctions.

Calenduloside E Ameliorates Myocardial Ischemia-Reperfusion Injury through Regulation of AMPK and Mitochondrial OPA1.

Calenduloside E (CE) is a natural triterpenoid saponin isolated from Aralia elata (Miq.) Seem., a well-known traditional Chinese medicine. Our previous studies have shown that CE exerts cardiovascular protective effects both in vivo and in vitro. However, its role in myocardial ischemia/reperfusion injury (MIRI) and the mechanism involved are currently unknown. Mitochondrial dynamics play a key role in MIRI. This study investigated the effects of CE on mitochondrial dynamics and the signaling pathways involved in myocardial ischemia/reperfusion (MI/R). The MI/R rat model and the hypoxia/reoxygenation (H/R) cardiomyocyte model were established in this study. CE exerted significant cardioprotective effects in vivo and in vitro by improving cardiac function, decreasing myocardial infarct size, increasing cardiomyocyte viability, and inhibiting cardiomyocyte apoptosis associated with MI/R. Mechanistically, CE restored mitochondrial homeostasis against MI/R injury through improved mitochondrial ultrastructure, enhanced ATP content and mitochondrial membrane potential, and reduced mitochondrial permeability transition pore (MPTP) opening, while promoting mitochondrial fusion and preventing mitochondrial fission. However, genetic silencing of OPA1 by siRNA abolished the beneficial effects of CE on cardiomyocyte survival and mitochondrial dynamics. Moreover, we demonstrated that CE activated AMP-activated protein kinase (AMPK) and treatment with the AMPK inhibitor, compound C, abolished the protective effects of CE on OPA1 expression and mitochondrial function. Overall, this study demonstrates that CE is effective in mitigating MIRI by modulating AMPK activation-mediated OPA1-related mitochondrial fusion.

TNM-PNI: a novel prognostic scoring system for patients with gastric cancer and curative D2 resection.

PURPOSE: Gastric cancer (GC) is one of the most common malignancies and has a high mortality rate. In recent years, several nutritional or inflammatory biomarkers have been shown to effectively predict the prognosis of tumors. In this study, we intended to establish a prognostic scoring system for GC patients. PATIENTS AND METHODS: Our study included a total of 501 GC patients who were diagnosed with GC stage I-III and received curative gastrectomy with D2 lymphadenectomy between January 2011 and December 2012. Survival analysis was performed using Kaplan-Meier and log-rank tests. Two Cox multivariate models, one for continuous and one for categorical variables, were established to identify independent prognostic factors. All statistical analyses were performed using SPSS 20.0. RESULTS: Univariate and multivariate analyses revealed that tumor-node-metastasis (TNM) stage, preoperative prognostic nutritional index (PNI), and adjuvant therapy were independent prognostic factors for GC patients. We established a new composite variable, TNM-PNI, which was confirmed to be a major prognostic factor for curative D2 resection, independent of whether adjuvant therapy was administered. GC patients with higher TNM-PNI scores always had worse cancer outcomes. In addition, we found that adjuvant therapy might be beneficial for the survival of GC patients with TNM-PNI =4 or 5. CONCLUSION: Preoperative PNI plays a distinctly subsidiary role to the TNM stage when predicting patient prognosis. TNM-PNI is a novel and an effective prognostic index for GC patients with curative D2 resection and a good supplement for the National Comprehensive Cancer Network Guidelines.