Major depressive disorder (MDD) is characterized by mood, vegetative, cognitive, and even psychotic symptoms and signs that can cause substantial impairments in quality of life and functioning. Up to now, the exact pathogenesis of MDD remains poorly understood. Recent research has begun to reveal that the pro-inflammatory cytokines, particularly, tumor necrosis factor-α (TNF-α), play an integral role in the pathophysiology of depressive disorders and the mechanism of antidepressant treatment. On the base of several observations: it is found that subsets of MDD patients have enhanced plasma levels TNF-α; antidepressant treatments had linked with the decline of TNF-α; central administration of TNF-α gives rise to sickness behavior which shares features with depression; and a blockade of it can ameliorate depressive symptomatology in animal models and clinical trials. In this review article, we focus on recent evidence linking TNF-α and MDD looking at data from animal and clinical studies, illustrating the pathophysiological role, susceptibility and its therapeutic application in depression. We conclude by discussing future directions for research, in particular the opportunities for the development of novel therapeutics that target TNF-α. This will be very important for designing preventative strategies and for the identification of new drug targets and preventative strategies.

Ellagic acid (EA) is a kind of polyphenol compound extracted from a variety of herbs, such as paeoniae paeoniae, raspberry, Chebule, walnut kernel, myrrh, loquat leaf, pomegranate bark, quisquite, and fairy herb. It has anti-tumor, anti-oxidation, anti-inflammatory, anti-mutation, anti-bacterial, anti-allergic and multiple pharmacological properties. Studies have shown its anti-tumor effect in gastric cancer, liver cancer, pancreatic cancer, breast cancer, colorectal cancer, lung cancer and other malignant tumors, mainly through inducing tumor cell apoptosis, inhibiting tumor cell proliferation, inhibiting tumor cell metastasis and invasion, inducing autophagy, affecting tumor metabolic reprogramming and other forms of anti-tumor efficacy. Its molecular mechanism is mainly reflected in inhibiting the proliferation of tumor cells through VEGFR-2 signaling pathway, Notch signaling pathway, PKC signaling pathway and COX-2 signaling pathway. PI3K/Akt signaling pathway, JNK (cJun) signaling pathway, mitochondrial pathway, Bcl-2 / Bax signaling pathway, TGF-β/Smad3 signaling pathway induced apoptosis of tumor cells and blocked EMT process and MMP SDF1α/CXCR4 signaling pathway inhibits the metastasis and invasion of tumor cells, induces autophagy and affects tumor metabolic reprogramming to produce anti-tumor effects. At present, the analysis of the anti-tumor mechanism of ellagic acid is slightly lacking, so this study comprehensively searched the literature on the anti-tumor mechanism of ellagic acid in various databases, reviewed the research progress of the anti-tumor effect and mechanism of ellagic acid, in order to provide reference and theoretical basis for the further development and application of ellagic acid.

Depression pertains to the category of "Emotional Diseases" in traditional Chinese medicine (TCM). Its clinical symptoms are similar to the manifestations of "lily disease" from the TCM classics Synopsis of the Golden Chamber written by Zhang Zhongjing in the Han Dynasty. Also in this book, Lily Bulb and Rehmannia Decoction (LBRD) is the formula for the treatment of "lily disease". The classical herbal formula LBRD is composed of two herbs lily bulb and fresh rehmannia juice, with the function of nourishing yin and replenishing heart and lung. It has been clinically applied to treat "lily disease" for two thousand years. In this review, we focused on recent evidence linking LBRD and depression extracting data from animal and clinical studies, summarizing the primitive dosage and producing area of genuine medicinal materials of LBRD, clinical application, pharmacological mechanism and the effective substance basis for the treatment of depression. In conclusion, we discussed existing problems and future perspective. This systematic review will seek to enhance our understanding about pharmacology mechanism, herb-prescribing and recipe-constructing, and the development of novel formula for depression treatments.

Gout is a common arthritis condition due to disorders of purine metabolism and decreased uric acid excretion. Although researchers have carried out various studies on this disease, there are no effective drugs for patients with gout. In traditional Chinese medicine (TCM), gout pertains the category of Bi pattern due to qi stagnation in the meridians and collaterals. Chinese herbal medicinals has been employed to treat Bi patterns since the ancient China. In recent decades, classical TCM formulas and agents isolated from some Chinese herbal medicinals have been applied to treat gout and have achieved satisfactory effect. In this review, we focus on recent studies of gout in which TCM formulas were applied to treat animal models or to treat patients, and summarize the mechanism of gout from TCM perspective, the clinical application, pharmacological mechanism and the chemical compounds of TCM formulas in treating gout. In conclusion, through this study, we summarized the application principle of TCM formulas in gout treatment and some key issues of current research, and we hope this study will provide some references for applying TCM formulas to treat gout and will lay a foundation for the development of novel formulas for gout treatments.

Major depression is a prevalent mood disorder. Chronic stress is presumably main etiology that leads to the neuron and synapse atrophies in the limbic system. However, the intermediate molecules from stresses to neuronal atrophy remain elusive, which we have studied in the medial prefrontal cortices from depression mice. The mice were treated by the chronic unpredictable mild stress (CUMS) until they expressed depression-like behaviors confirmed by the tests of sucrose preference, forced swimming and Y-maze. High-throughput sequencings of microRNA and mRNA in the medial prefrontal cortices were performed in CUMS-induced depression mice versus control mice to demonstrate the molecular profiles of major depression. In the medial prefrontal cortices of depression-like mice, the levels of mRNAs that translated the proteins for the GABAergic synapses, dopaminergic synapses, myelination, synaptic vesicle cycle and neuronal growth were downregulated. miRNAs of regulating these mRNAs are upregulated. The deteriorations of GABAergic and dopaminergic synapses as well as axonal growth are associated with CUMS-induced depression.

BACKGROUND:We sought to determine by meta-analysis the relationship between drinking alcohol and the risk of gastric cancer. MATERIAL AND METHODS:A systematic Medline search was performed to identify all published reports of drinking alcohol and the ...