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Autophagy is a protective mechanism important in human diseases as cancer. We evaluated the impact of khalas date extract (KDE) (20-60 mg/mL) on cell viability, morphological changes, DNA fragmentation and gene expression of LC3B-II associated with autophagosome on HepG2 cell line. The GC/MS identification of KDE showed its high content of flavonoids including quercetin, myricetin, kaempferol and catechol. KDE reduced cell viability of HepG2 with IC50 (31.52 mg/mL). Cells treated with KDE showed two band of DNA fragments at (30 and 40 mg) indicating that KDE induced DNA damage and apoptosis in HepG2. The analysis RT-PCR data showed a 0.2-fold increase in the expression of LC3-B in the cells treated with KDE versus control. We concluded that, KDE flavonoids such as quercetin, myricetin kaempferol exhibited anticancer properties manifested by inhibition of HepG2 cell viability and induction of apoptosis and upregulation of the pro-autophagy LC3-B gene.

Serum total and free calcium reflect the status of the body health and disease. Smoking is risk factor for many diseases as cardiovascular, lung, and cancers. The goal of this work is to evaluate the correlation between serum lead, cadmium arsenate resulting from passive smoking, and bone status in females. This study was conducted on two hundred women (age 30-50 years) divided into four groups (each 50). Group I, control, included non-smoking healthy women. Group II included heavy smoker (20 cigarettes/day). Group III, nonsmoker women with osteoporosis, have many fractures. Group IV, smoking women with osteoporosis, included heavy smokers (20 cigarettes/day) with osteoporotic women and have many fractures. Data obtained showed that T-score of osteoporotic smokers was -3.5 that indicated reduced bone mineral density (BMD) while serum total and ionized calcium were statistically significant decreased in smokers with or without osteoporosis compared with nonsmokers (p0.001). A negative correlation between total and free calcium and cadmium levels in smokers was compared with nonsmokers (r =-0.65). The levels of C-terminal pro-peptide of pro-collagen type I (PICP) and N-terminal pro-peptide of procollagen type I (PINP) were higher in smoker osteoporotic women than nonsmokers. It was concluded that cadmium resulting from smoking may compete with absorption of calcium and reduced its level and BMD and increased incidence of osteoporosis. The elevated PICP and PINP indicated decreased rate of proto collagen I turnover in bone tissue and increased incidence of osteoporosis.

Natural polyamines such as putrescine, spermidine, and spermine are crucial in the cell proliferation and maintenance in all the eukaryotes. However, the requirement of polyamines in tumor cells is stepped up to maintain tumorigenicity. Many synthetic polyamine analogues have been designed recently to target the polyamine metabolism in tumors to induce apoptosis. N 4 -Erucoyl spermidine (designed as N 4 -Eru), a novel acylspermidine derivative, has been shown to exert selective inhibitory effects on both hematological and solid tumors, but its mechanisms of action are unknown. In this study, RNA sequencing was performed to investigate the anticancer mechanisms of N 4 -Eru-treated T-cell acute lymphoblastic leukemia (ALL) cell line (Jurkat cells), and gene expression was examined through different tools. We could show that many key oncogenes including NDRG1, CACNA1G, TGFBR2, NOTCH1,2,3, UHRF1, DNMT1,3, HDAC1,3, KDM3A, KDM4B, KDM4C, FOS , and SATB1 were downregulated, whereas several tumor suppressor genes such as CDKN2AIPNL, KISS1, DDIT3, TP53I13, PPARG, FOXP1 were upregulated. Data obtained through RNA-Seq further showed that N 4 -Eru inhibited the NOTCH/Wnt/JAK-STAT axis. This study also indicated that N 4 -Eru-induced apoptosis could involve several key signaling pathways in cancer. Altogether, our results suggest that N 4 -Eru is a promising drug to treat ALL.

Diabetes Mellitus is a chronic, lifelong disease currently impacting people throughout the world. A fundamental cause of Diabetes Mellitus: Non-enzymatic protein glycosylation (glycation) contributes to a group of metabolic diseases, including diabetes-associated late complications, atherosclerosis, chronic renal failure, Alzheimer’s disease and inflammatory arthritis. It has been hypothesized that inhibition of glycation may prevent the diseases associated with diabetes. Inhibitors of glycation have been explored for several decades, chiefly using in vitro models, which resulted in discovery of different natural compounds capable of forestalling glycation, such as antioxidants, polysaccharide, metal chelators and peptides. Many peptides released from different proteins have proven to possess physiological functions besides their nutrient roles. Even the results of in vitro studies are not directly applicable on the in vivo situation due to differences in the conditions, mechanism of glycation and bioavailability issues. In this review article, we briefly discuss the mechanism of advanced glycation end products (AGEs) in promoting pathogenesis and then present the recent findings concerning the role of plant-based inhibitors and amino acid peptides in decreasing the formations of AGEs. These findings suggest that enrichment of diet with natural, anti-glycating agents may reduce glycation and as a consequence, diabetic complications. Keywords: Glycation, Diabetes, Hyperglycemia, AGEs-inhibitors, Retinopathy.