Benzyl isothiocyanate (BITC) is a member of the isothiocyanate compounds that found in cruciferous vegetables. BITC has a potential anticancer effect in different types of tumors. Few studies referred to the antineoplastic effect of BITC against HCC. The mechanism of BITC concerning retardation of HCC progression is incompletely understood. This study evaluated the role of HGF, pAkt and STAT3 in BITC induced HCC growth retardation. HCC was induced in mice using diethylnitrosamine (DEN) 75 mg/kg once a week for 4 weeks. BITC 10 and 20 mg/kg was given to mice orally each day for 10 weeks. The HCC cell lines HepG2 and Huh-7 were also used to evaluate the effect of BITC on tumor cells behavior. Immunoassay was used to detect expressions of caspase-3 activity, VEGF, MMP-2, TNF-α, HGF and pAkt. STAT3 expression was detected in liver tissues using immunohistochemical staining. BITC has a potential role in suppressing hepatic precancerous lesion progression in mice. The drug increased caspase-3 activity in tumor cells and inhibited the angiogenic marker VEGF. It also decreased the metastatic marker MMP-2. This anticancer effect of BITC was observed in DEN treated mice as well as in hepatoma cell lines. The reported antineoplastic activity was correlated with downregulation of HGF and its downstream molecules pAkt and STAT3. The effect of BITC on HGF /pAkt/ STAT3 axis has a potential role in both chemopreventive and chemotherapeutic effects of BITC.

Gastric ulcer is the most digestive disease found in clinical practice. Punicalagin (PCG) found in pomegranate juice has antioxidant and tissue repair properties. Therefore, the aim of this study was to investigate punicalagin’s gastroprotective effect against ethanol-induce gastric injury. Four groups of rats; first group served as control, group 2: Treated with absolute ethanol (5 ml/kg, po), group 3: Rats were pre-treated with ranitidine (as a reference drug) (50 mg/kg, po) before ethanol and group 4: Pre-treated with PCG (4 mg/kg, po) before ethanol. Pretreatment with PCG reduced ulcer index and histopathological changes, oxidative stress induced by ethanol while it elevated antioxidant activity. Although, it down regulated Tumor Necrosis Factor (TNF-α) gene expression and mucosal levels of inflammatory cytokines; TNF-α, Interleukin (IL-1β) and Interferon Gamma (IFNγ), it up regulated mucosal level of IL-10. Also, it reduced mucosal Nuclear Factor Kappa B (NFκB) protein expression, mylopeoxidase and caspase 3 activities as well as gene expression of caspase 9 while it elevated antiapoptotic B-Cell Lymphoma 2 (Bcl-2) gene expression, mucosal nitric oxide and mucin content. However, it had negative action on prostaglandin E2 and acid secretions. These findings indicate gastroprotective effects of punicalagin against ethanol induced gastric ulcer through suppression of mucosal oxidative stress and inflammation through NFκB pathway as well cytoprotective defences independent on prostaglandin E2 and acid secretions.

Background: Alzheimer’s disease (AD) is a chronic neurological illness that causes considerable cognitive impairment. Hepatic and renal dysfunction may worsen AD by disrupting β-amyloid homeostasis at the periphery and by causing metabolic dysfunction. Wheatgrass (Triticum aestivum) has been shown to have antioxidant and anti-inflammatory properties. This work aims to study the effect of aluminum on neuronal cells, its consequences on the liver and kidneys, and the possible role of fluoxetine and wheatgrass juice in attenuating these pathological conditions. Method: Rats were divided into five groups. Control, AD (AlCl₃), Fluoxetine (Fluoxetine and AlCl₃), Wheatgrass (Wheatgrass and AlCl₃), and combination group (fluoxetine, wheatgrass, and AlCl₃). All groups were assigned daily to different treatments for five weeks. Conclusions: AlCl₃ elevated liver and kidney enzymes, over-production of oxidative stress, and inflammatory markers. Besides, accumulation of tau protein and Aβ, the elevation of ACHE and GSK-3β, down-regulation of BDNF, and β–catenin expression in the brain. Histopathological examinations of the liver, kidney, and brain confirmed this toxicity, while treating AD groups with fluoxetine, wheatgrass, or a combination alleviates toxic insults. Conclusion: Fluoxetine and wheatgrass combination demonstrated a more significant neuroprotective impact in treating AD than fluoxetine alone and has protective effects on liver and kidney tissues.

Background: Triple-negative breast cancer (TNBC) is one of the most aggressive subtypes of breast cancer. TNBC lacks targeted therapy receptors, rendering endocrine and HER2-targeted therapies ineffective. TNBC is typically treated with cytotoxic chemotherapy followed by surgery. Targeting epigenetic modifications could potentially be a new effective TNBC target therapy. The aim of this study is to examine the effects of epigenetic drugs, decitabine as DNA methyltransferase inhibitor (DNMTI) and vorinostat as histone deacetylase inhibitor (HDACI), and the ERβ agonist DPN on ERα and ERβ re-expressions in the MDA-MB-231 cells as a model of TNBC. Methods: Using MTT assay, the IC₅₀ of decitabine, vorinostat, and DPN on MDA-MB-231 cells were determined. The effects of all drugs alone or in combinations on MDA-MB-231 cells were evaluated. qRT-PCR was used to determine ERα & ERβ gene expression. Caspase-3 activity and the protein expression levels of VEGF, Cyclin D1, and IGF-1 were assessed. Results: Both ERα and ERβ mRNA were re-expressed in different high levels in all treated groups, especially in the triple therapy group compared with control. Significantly, the triple drugs therapy showed the lowest levels of VEGF, Cyclin D1, and IGF-1 and the highest level of Caspase-3 activity, indicating a possible antitumor effect of ERβ activation through decreasing proliferation and angiogenesis and increasing apoptosis in MDA-MB-231 cells. Conclusions: The antiproliferative effect of ERβ could be retained when co-expressed with Erα using a powerful epigenetic combination of Decitabine and vorinostat with DPN.