PURPOSE: Breast cancer is the most common type of cancer in women. Despite various pharmacological developments, the identification of new therapies is still required for treating breast cancer. Crab is often recommended as a traditional medicine for cancer. This study aimed to determine the in vitro effect of a hydroalcoholic crab shell extract on a breast cancer cell line. METHODS: In this experimental study, MCF7 breast cancer cell line was used. Crab shell was powdered and a hydroalcoholic (70degrees ethanol) extract was prepared. Five concentrations (100, 200, 400, 800, and 1,000 microg/mL) were added to the cells for three periods, 24, 48, and 72 hours. The viability of the cells were evaluated using trypan blue and 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays. Cell apoptosis was determined using the terminal deoxynucleotidyl transferase dUTP nick end labeling method. Nitric oxide (NO) level was assessed using the Griess method. Data were analyzed using analysis of variance, and p<0.05 was considered significant. RESULTS: Cell viability decreased depending on dose and time, and was significantly different in the groups that were treated with 400, 800, and 1,000 microg/mL doses compared to that in the control group (p<0.001). Increasing the dose significantly increased apoptosis (p<0.001). NO secretion from MCF7 cells significantly decreased in response to different concentrations of the extract in a dose- and time-dependent manner (p<0.050). CONCLUSION: The crab shell extract inhibited the proliferation of MCF7 cells by increasing apoptosis and decreasing NO production.
Apoptosis ; Breast Neoplasms* ; Cell Line* ; Cell Survival ; DNA Nucleotidylexotransferase ; Female ; Humans ; MCF-7 Cells ; Medicine, Traditional ; Nitric Oxide ; Trypan Blue

Alzheimer disease (AD) is a common neurodegenerative disorder, characterized by memory impairment, dementia, and diminished cognitive function. This disease affects more than 20 million people worldwide. Amyloid beta (Aβ) plaques and neurofibrillary tangles (NFTs) are important pathological markers of AD. Multiple studies have indicated a potential association between elevated cholesterol levels and increased risk of AD, suggesting that lowering the cholesterol level could be a viable strategy for AD treatment or prevention. Statins, potent inhibitors of cholesterol synthesis, are widely used in clinical practice to decrease the plasma levels of LDL cholesterol in patients with hyperlipidemia. Statins are known to play a neuroprotective role in limiting Aβ pathology through cholesterol-lowering therapies. In addition to Aβ plaques and neurofibrillary tangles, the brains of AD patients exhibit signs of oxidative stress, neuroinflammatory responses, and synaptic disruption.Consequently, compounds with antioxidant, anti-inflammatory, and/or neuroprotective properties could be beneficial components of AD treatment strategies. In addition to lowering LDL cholesterol, statins have demonstrated therapeutic efficacy in various forms, including antioxidant, anti-inflammatory, and neuroprotective effects. These properties of statins are potential mechanisms underlying their beneficial effects in treating neurodegenerative diseases. Therefore, this review was conducted to provide an overview of the protective effects of statins against AD.