Background: In this study, the aqueous extract of Anethum graveolens (dill) leaves was studied for its effects on treating convulsions and epilepsy, by using a pentylenetetrazole (PTZ) kindling model. The evaluated plant has a traditional medical reputation for profound anticonvulsant activities, additionally, dill has been claimed to exhibit anti-inflammatory and analgesic properties. Methods: For the PTZ kindling induction, mice were given a dose of PTZ (37 mg/kg, intraperitoneally) every other day, and seizure stages were precisely recorded. During and after kindling, the effects of the non-toxic doses of the aqueous extracts (100, 250, and 400 mg/kg) on seizure latency in stage 2 (S2L), seizure latency in stage 4 (S4L), and seizure duration in stage 5 (S5D) were measured. Results: The aqueous extract of dill leaves had a noticeable anticonvulsant effect. The 400 mg/kg dose of the extract sample decreased with S5D (P < 0.05), and increased with S2L and S4L significantly (P < 0.05 and P < 0.01, respectively). Conclusion: The obtained data shows that the aqueous extract possesses anticonvulsant activity against seizure induced by PTZ. The presence of anticonvulsant compounds in this medicinal herb suggests further activity and guided fractionation studies in order to introduce this plant as a valuable source of anticonvulsant agents.
Anethum graveolens ; Anticonvulsants ; Pentylenetetrazole

PURPOSE: MicroRNAs (miRNAs) have received much attention owing to their aberrant expression in various stages of cancer. In many biological processes, miRNAs negatively regulate gene expression, and may be useful in therapeutic strategies. The present study evaluated the effects of silibinin (silybin), a natural flavonoid, on miRNA expression and attempted to elucidate therapeutic targets in MCF-7 breast cancer cells. METHODS: The rates of cell proliferation and apoptosis were determined in silibinin-treated and untreated MCF-7 cells. Furthermore, the expression levels of miR-21 and miR-155 were measured in MCF-7 cells after incubation with silibinin (100 µg/mL), and the putative targets of the miRNAs within the apoptotic pathways were predicted using bioinformatic approaches. The expression levels of some of these targets were evaluated by quantitative reverse transcription polymerase chain reaction (qRT-PCR). RESULTS: Silibinin induced apoptosis in MCF-7 cells in a dose- and time-dependent manner. qRT-PCR analysis revealed a decrease in miR-21 and miR-155 expression levels in silibinin-treated cells relative to the levels in the untreated cells. Potential miR-21 and miR-155 targets within the apoptotic pathways, such as CASP-9, BID, APAF-1, CASP-3, CASP-8, and PDCD4, were predicted by in silico analysis. qRT-PCR analysis showed upregulation of some of these potential targets including caspase-9 (CASP-9) and BID after silibinin treatment for 48 hours. CONCLUSION: Our results suggest a correlation between the expression of miR-21 and miR-155, and MCF-7 cell proliferation. The antiproliferative activity of silibinin may partly be attributable to the downregulation of miR-21 and miR-155, and the upregulation of their apoptotic targets. Furthermore, the upregulation of CASP-9 and BID indicates that silibinin induces apoptosis through both the extrinsic and intrinsic pathways.
Apoptosis* ; Biological Processes ; Breast Neoplasms* ; Breast* ; Caspase 9 ; Cell Proliferation ; Computer Simulation ; Down-Regulation* ; Gene Expression ; Humans* ; MCF-7 Cells ; MicroRNAs ; Polymerase Chain Reaction ; Reverse Transcription ; Up-Regulation

Background: Auraptene is a simple coumarin that exhibits multiple protective activities in the brain. Alzheimer’s disease is a complex, multifactorial, and progressive neurodegenerative disease. Microinjection of the β-amyloid peptide (Aβ) into the hippocampus of rat has been recognized as a reliable and stable animal model of Alzheimer’s disease, which mimics the memory deficits. In the present study, the memory enhancing effects of auraptene were studied in rats that Aβ was injected into their hippocampus to create a model of Alzheimer’s disease. Methods: Different doses of auraptene (5, 10 and 25 mg/kg) were administered intraperitoneally to male Wistar rats. The spatial memory performance was tested by Morris water maze after Alzheimer`s induction. The hippocampal expression of pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins were calculated for evaluating the neuroprotective and anti-apoptotic effects of Auraptene in the brain tissue. Results: In comparison with the control group, auraptene significantly decreased the escape latency time in the treated rats. In addition, auraptene increased the percentage of time spent and traveled pathway in the target quadrant. Molecular data showed that auraptene attenuated the Bax/Bcl-2 ratio in the hippocampus of rats. Conclusion: This study demonstrated the memory enhancing effect of Aur after Aβ injection, which could be through inhibiting the apoptotic pathways in the hippocampus of rats.