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cell metastasis was reversed. CONCLUSION Jinfukang inhibits the metastasis of CTC-TJH-01 cells through the EGF pathway. ETHNOPHARMACOLOGICAL RELEVANCE Withania somnifera (L.) Dunal also known as 'Ashwaghanda' in Sanskrit and as 'Indian Winter Cherry' in english. is an important medicinal herb in India. It is widely used in Indian systems of medicine as an adaptogen, nerve tonic, anti-stress, memory enhancer and against cognitive deficits, insomnia, anxiety, infectious diseases, infertility, rheumatoid arthritis and gout over thousands of years. Its formulations are mainly used in Unani and Ayurvedic system of medicine. It is a remarkable centuries old herbal Rasayana used to treat neuronal ailments and is known as ''Sattvic Kapha Rasayana. AIM OF THE STUDY To review neuroprotective properties of Withania somnifera (L.)extract as well as its active constituents in neurodegenerative diseases and other neurological ailments. MATERIALS AND METHODS The sources of information used in present article include Indian system of Medicine reports on the use of natural products, Medicinal books, research articles and scientific databases like PubMed, Google Scholar, Web of Science, Science-Direct, SciFinder, ACS Publications and Wiley Online Library. RESULTS Research reports based largely on preclinical studies as well as few clinical trials have highlighted the neuroprotective role of Ashwagandha against many neurodegenerative diseases including Alzheimer's, Huntington's and Parkinson's disease. The protective effects of Ashwagandha were accomplished by restoring mitochondrial and endothelial function, mitigation of apoptosis, inflammation and oxidative stress mechanisms. CONCLUSION In this review, we recapitulated neuroprotective properties of Ashwagandha extracts and/or its major constituents and discussed their mechanisms of action and potential therapeutic applications. The pre-clinical as well as clinical studies suggest the use of Withania somnifera (L.) against neurodegenerative disease. However, extensive studies are warranted to validate the use of extract or its single constituents for its clinical use. ETHNOPHARMACOLOGICAL RELEVANCE Terminalia catappa L. (Combretaceae), known as "amendoeira da praia" in Brazil, has been recognized as a medicinal plant in folk medicine for the treatment of gastrointestinal disorders and other inflammatory conditions. The present study aimed to investigate the preventive and healing effects of the infusion of leaves of T. catappa (ILTC) against gastric lesions caused by ischemia and reperfusion (I/R) injury and characterize its mechanism of action in the gastric mucosa of rats. MATERIALS AND METHODS Different doses (30, 100, and 300 mg/kg) of ILTC were orally administered as acute and subacute treatments against I/R-induced gastric lesion in rats. After treatment, the stomach of rats was collected to measure the lesion area, redox parameters malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH) and inflammatory parameters myeloperoxidase activity (MPO), interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α). The activities of matesions in rats. By decreasing MPO levels, ILTC enabled the action of MMP-2, which led to tissue recovery in the gastric mucosa. Lumbar degenerative disc disease (DDD) is a multifaceted progressive condition and often accompanied by disc herniation (DH) and/or degenerative spondylolisthesis (DS). Given the high prevalence of the disease (up to 20% according to some estimates) and the high costs associated with its care, there is a need to explore novel therapies such as regenerative medicine. Exploring these novel therapies first warrants investigation of molecular pathways underlying these disorders. Here, we show results from next generation RNA sequencing (RNA-seq) on mRNA isolated from 10 human nucleus pulposus (NP) samples of lumbar degenerated discs (DH and DS; n=5 for each tissue) and other musculoskeletal tissues (Bone, cartilage, growth plate, and muscle; n=7 for each tissue). Pathway and network analyses based on gene ontology (GO) terms were used to identify the biological functions of differentially expressed mRNAs. A total of 701 genes were found to be significantly upregulated in lumbar NP tissue compared to other musculoskeletal tissues. These differentially expressed mRNAs were primarily involved in DNA damage, immunity and G1/S transition of mitotic cell cycle. Interestingly, DH-specific signaling genes showed major network in chemotactic (e.g., CXCL10, CXCL11, IL1RL2 and IL6) and matrix-degrading pathway (e.g., MMP16, ADAMTSL1, 5, 8, 12, and 15), while DS-specific signaling genes were found to be those involved in cell adhesion (e.g., CDH1, EPHA1and EFNA2) and inflammatory cytokines (e.g., CD19, CXCL5, CCL24, 25 and XCL2). Our findings provide new leads for therapeutic drug discovery that would permit optimization of medical or pharmacological intervention for cases of lumbar DDD. V.BACKGROUND Several studies have examined the association between transforming growth factor-β (TGF-β) genetic polymorphisms and chronic obstructive pulmonary disease (COPD) risk, but the results remained inconclusive and controversial. Ivacaftor ic50 AIMS We aimed to examine the correlation between TGF-β genetic polymorphisms and COPD risk through a comprehensive meta-analysis. Additionally, changes in circulating TGF-β concentrations across genotypes of TGF-β genetic polymorphisms were analyzed. METHODS Literature search, quality assessment, and data extraction were completed independently and in duplicate. Data are expressed in odds ratio (OR) or weighted mean difference (WMD) with 95% confidence interval (CI). RESULTS A total of 12 articles, involving 14 independent studies and 7 170 participants, were meta-analyzed for the correlation of five polymorphisms (rs2241712, rs1800469, rs1982073, rs6957, and rs2241718) in TGF-β gene with COPD risk. Under the allele model, no statistical significance was observed for all polymorphisms associated with COPD risk. Subsidiary analyses indicated that country, COPD stage, and diagnosis of COPD were potential sources of between-study heterogeneity. Filled full plots revealed no missing studies for all studied polymorphisms, except rs1982073. Genotype-phenotype analyses showed that carriers of rs1800469 CT genotype had significantly higher concentrations of circulating TGF-β than those with CC genotype in COPD patients (WMD 0.28 pg/ml, 95% CI 0.01 to 0.56). CONCLUSION Our findings failed to support the candidacy of TGF-β gene in the development of COPD, whereas the contribution of TGF-β gene to COPD might be ethnicity- and stage-dependent.
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