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MicroRNAs (miRNAs) are of interest because they are dysregulated in different diseases, including liver diseases. MicroRNA-122 is an organ specific miRNA representing 70% of total miRNA in hepatocytes. The aim of this study was to investigate serum miRNA-122 expression in Egyptian patients with non-alcoholic fatty liver disease (NAFLD) and to determine its relationship with insertion/deletion polymorphism within the 3′ UTRs regions of interleukin-1A (IL-1A) gene which represents the binding site of miRNA-122. The study included 75 healthy subjects and 75 patients with NAFLD. Patients were recruited from the internal medicine outpatient clinic at Suez Canal University Hospital, Ismailia, Egypt. Serum miRNA-122 expression was determined using quantitative real-time PCR and normalization was done against RNU6B as an internal control. Our results reveled that about 76% of patients exhibited up-regulation of miRNA-122. The median miRNA-122 expression level in patients increased significantly (6.68 fold) compared to control (p = 0.001). Serum miRNA-122 expression level in NAFLD patients showed positive correlation with both serum triglycerides (TG) and very low density lipoprotein-cholesterol (VLDL-C) level (p = 0.048), and with serum IL-1A (p = 0.03). Regarding the relation between serum miRNA-122 expression and different genotypes of IL-1A insertion/deletion gene polymorphism (DD, ID, and II genotypes), patients carrying the major high risk DD genotype had a significant increase in miRNA-122 expression than those with heterozygous ID and the homozygous II genotypes (p = 0.002). In conclusion, serum miRNA-122 expression showed positive association with increased susceptibility to NAFLD in the study population. Insertion/deletion IL-1A gene polymorphism may be a marker for genetic susceptibility to NAFLD in Egyptian population, likely through miRNA-122 mediated regulation.


Gingerol is a major dietary compound that occurs in several plants belonging to the Zingiberaceae family. In the current study, the protective effect of gingerol on STZ-induced sporadic Alzheimer’s disease (SAD) was determined. Gingerol was isolated from the seeds of Aframomum melegueta K. Schum and tested at doses of 10 and 20 mg/kgbwt for its possible effect on the SAD model in mice, using celecoxib (30 mg/kg bwt) as a reference standard. The curative effects of gingerol were assessed through measurement of β-amyloid (Aβ-42), α-, β- secretases, APH1a and COX-2 levels. In addition, improvement in the cognitive deficit in mice after treatment was confirmed using the water maze and Y-maze with intra-maze cues. Gingerol improved the cognitive and behavioral impairment and AD-like pathology in streptozotocin model mice. These beneficial effects occurred with an increase in α-secretase activity and a decrease in cerebral Aβ-42, β- secretase, APH1a activity and COX-2-linked neuro-inflammation.


The salivary glands of animals have great potential to act as powerful bioreactors to produce human therapeutic proteins. Human nerve growth factor (hNGF) is an important pharmaceutical protein that is clinically effective in the treatment of many human neuronal and non-neuronal diseases. In this study, we generated 18 transgenic (TG) founder mice each carrying a salivary gland specific promoter-driven hNGF transgene. A TG mouse line secreting high levels of hNGF protein in its saliva (1.36 μg/mL) was selected. hNGF protein was successfully purified from the saliva of these TG mice and its identity was verified. The purified hNGF was highly functional as it displayed the ability to induce neuronal differentiation of PC12 cells. Furthermore, it strongly promoted proliferation of TF1 cells, above the levels observed with mouse NGF. Additionally, saliva collected from TG mice and containing unpurified hNGF was able to significantly enhance the growth of TF1 cells. This study not only provides a new and efficient approach for the synthesis of therapeutic hNGF but also supports the concept that salivary gland from TG animals is an efficient system for production of valuable foreign proteins.

Puerarin ameliorated the behavioral deficits induced by chronic stress in rats

Posted by Zhi-Kun Q, Guan-Hua Z, De-Sheng Z, et al. on 2017-08-14 22:56:51


The present study aimed to investigate the mechanisms underlying the antidepressant-like effects of puerarin via the chronic unpredictable stress (CUS) procedure in rats. Similar to Sertraline (Ser), Chronic treatment of puerarin (60 and 120 mg/kg, i.g) elicited the antidepressant-like effects by reversing the decreased sucrose preference in sucrose preference test (SPT), by blocking the increased latency to feed in novelty-suppressed feeding test (NSFT) and the increased immobility time in forced swimming test (FST) without affecting locomotor activity. However, acute puerarin treatment did not ameliorate the antidepressant- and anxiolytic- like effects in FST and NSFT, respectively. In addition, enzyme linked immunosorbent assay (ELISA) and high performance liquid chromatography-electrochemical detection (HPLC-ECD) showed that chronic treatment of puerarin (60 and 120 mg/kg, i.g) reversed the decreased levels of progesterone, allopregnanolone, serotonin (5-HT) and 5-Hydroxyindoleacetic acid (5-HIAA) in prefrontal cortex and hippocampus of post-CUS rats. Furthermore, puerarin (60 and 120 mg/kg, i.g) blocked the increased corticotropin releasing hormone (CRH), corticosterone (Cort) and adrenocorticotropic hormone (ACTH). Collectively, repeated administration of puerarin alleviated the behavioral deficits induced by chronic stress which was associated with the biosynthesis of neurosteroids, normalization of serotonergic system and preventing HPA axis dysfunction.

ACF7 regulates inflammatory colitis and intestinal wound response by orchestrating tight junction dynamics

Posted by Yanlei M, Jiping Y, Chenzhang S, et al. on 2017-08-14 20:07:01


In the intestinal epithelium, the aberrant regulation of cell/cell junctions leads to intestinal barrier defects, which may promote the onset and enhance the severity of inflammatory bowel disease (IBD). However, it remains unclear how the coordinated behaviour of cytoskeletal network may contribute to cell junctional dynamics. In this report, we identified ACF7, a crosslinker of microtubules and F-actin, as an essential player in this process. Loss of ACF7 leads to aberrant microtubule organization, tight junction stabilization and impaired wound closure in vitro. With the mouse genetics approach, we show that ablation of ACF7 inhibits intestinal wound healing and greatly increases susceptibility to experimental colitis in mice. ACF7 level is also correlated with development and progression of ulcerative colitis (UC) in human patients. Together, our results reveal an important molecular mechanism whereby coordinated cytoskeletal dynamics contributes to cell adhesion regulation during intestinal wound repair and the development of IBD.

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