Alzheimer’s disease is regarded as a common neurodegenerative disease that may lead to dementia and the loss of memory. We report here the nootropic and anti-amnesic effects of both peppermint and rosemary oils using a rat model of scopolamine-induced amnesia-like AD. Rats were administered orally with two doses (50 and 100 mg/kg) of each single oil and combined oils. The positive group used donepezil (1 mg/kg). In the therapeutic phase, rats were administered scopolamine (1 mg/kg) through the oral administration of oils. During the nootropic phase, both oils showed a significant (p < 0.05) decrease in radial arm maze latency times, working memory, and reference memory errors compared with the normal group, along with significant (p < 0.05) enhancements of long-term memory during the passive avoidance test. Therapeutic phase results revealed significant enhancements of memory processing compared with the positive groups. In the hippocampus, oils exhibited an elevation of BDNF levels in a dose-dependent manner. Immunohistochemistry findings showed increased hippocampal neurogenesis suppressed by scopolamine in the sub-granular zone, and the anti-amnesic activity of single oil was enhanced when the two oils combined. Gas chromatography–mass spectrometry (GCMS) of the two oils revealed sufficient compounds (1,8-Cineole, α-Pinene, menthol and menthone) with potential efficacy in the memory process and cognitive defects. Our work suggests that both oils could enhance the performance of working and spatial memory, and when combined, more anti-amnesic activity was produced. A potential enhancement of hippocampal growth and neural plasticity was apparent with possible therapeutic activity to boost memory in AD patients.

The epigenetic silencing of tumor suppressor genes (TSGs) is critical in the development of chronic myeloid leukemia (CML). SHP-1 functions as a TSG and negatively regulates JAK/STAT signaling. Enhancement of SHP-1 expression by demethylation provides molecular targets for the treatment of various cancers. Thymoquinone (TQ), a constituent of Nigella sativa seeds, has shown anti-cancer activities in various cancers. However, TQs effect on methylation is not fully clear. Therefore, the aim of this study is to assess TQs ability to enhance the expression of SHP-1 through modifying DNA methylation in K562 CML cells. The activities of TQ on cell cycle progression and apoptosis were evaluated using a fluorometric-red cell cycle assay and Annexin V-FITC/PI, respectively. The methylation status of SHP-1 was studied by pyrosequencing analysis. The expression of SHP-1, TET2, WT1, DNMT1, DNMT3A, and DNMT3B was determined using RT-qPCR. The protein phosphorylation of STAT3, STAT5, and JAK2 was assessed using Jess Western analysis. TQ significantly downregulated the DNMT1 gene, DNMT3A gene, and DNMT3B gene and upregulated the WT1 gene and TET2 gene. This led to hypomethylation and restoration of SHP-1 expression, resulting in inhibition of JAK/STAT signaling, induction of apoptosis, and cell cycle arrest. The observed findings imply that TQ promotes apoptosis and cell cycle arrest in CML cells by inhibiting JAK/STAT signaling via restoration of the expression of JAK/STAT-negative regulator genes.

Patients with chronic kidney disease (CKD) are prone to haemorrhage and/or thrombi formation, suggesting abnormalities in haemostasis. The study aimed to investigate the impairment of coagulation factors in CKD patients. One hundred and twenty-three (123) CKD patients, who were attending Prince Hamza and Al-Karak public hospitals, and fifty (50) healthy subjects (control) were recruited for the study. CKD patients were subcategorized according to their GFR value into III B and IV groups. Ethical approval was obtained, and all participants consented to the study. Whole blood samples were collected from all the CKD patients and 50 control (healthy) subjects and tested for prothrombin time (PT), activated partial thromboplastin time (aPTT), and coagulation factors I (fibrinogen), II, V, VII, VIII, IX, X, XI, and anti-thrombin III (ATIII) on STA coagulation analyzer. The levels of proteins C, S, and von Willebrand factor (VWF) were measured using enzyme-linked immunosorbent assay (ELISA). The findings showed a significant prolonged PT and aPTT in CKD patients compared to the control (healthy) subjects, and the level of F-V and F-XI were significantly decreased, justifying the clinical manifestation of bleeding in CKD patients. However, factors VII, VIII, and IX were increased significantly in CKD patients. The findings from this study have demonstrated that CKD impairs the coagulation factors and leads to an increase in the time required for clot formation, suggesting a tendency of patients with CKD to have frequent bleeding episodes.

Atherosclerosis is a disease of blood vessels which is caused by inherited and acquired factors and leads to different complications in the body including blood clot formation, a serious condition that can threat human life. This study aims to measure the prevalence of thrombophilia gene mutations; Factor V Leiden (FVL, G1691A) and F-II (G20210A) in Jordanian patients with atherosclerosis. Using real-time PCR, the prevalence of heterozygous and homozygous variants of FVL (G1691A) were 11.32 and 1.87% respectively. In F-II (G20210), the prevalence was 1.87 and 0.31% for heterozygous and homozygous variants, respectively. Comparing mutants’ frequencies between patients with atherosclerosis and healthy people (control) showed no significant difference suggesting no relation of these mutants and thrombus formation in atherosclerotic patients, however, among patients’ group there was a significant difference in the prevalence of FVL (G1691A) variants between male and female populations and insignificant difference for F-II (G20210). In conclusion, the results of this study showed no relation of inherited F-V and F-II gene mutations in blood clot formation in atherosclerotic patients, suggestion that blood clot formation is related only to environmental factors belong to the nature of atherosclerotic plaque which trigger platelets and clotting proteins activation.

Atherosclerosis is characterised by the deposition of lipids and cells in the intima layer of the blood vessels. Several diseases, genetic and environmental factors are combined with the progression of atherosclerosis such as hypertension, high plasma cholesterol, and single-nucleotide polymorphisms. A recent study revealed that STAT3, SLC11A1, CKAP4, IL1B, IL17RA, IL1RN, C5AR1, CXCL16, TLR2, and LYN genes are associated with atherosclerosis development and might be novel diagnostic biomarkers for this disease. In this study, we randomly selected STAT3, SLC11A1, CKAP4, IL1B, and IL17RA genes to measure their expression in patients with atherosclerosis. EDTA blood samples were collected from n=120 (one hundred atherosclerotic patients and twenty healthy people), RNA was extracted from samples and cDNA was constructed to perform real-time PCR. We observed that STAT3 and SLC11A1 expression significantly increased in the patient group compared with healthy people, and the expression of CKAP4, IL1B, and IL17RA genes was decreased but not significantly in patients with atherosclerosis. STAT3 and CKAP4 genes might be novel in the early diagnosis of atherosclerosis disease, especially in asymptomatic cases.