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Sesamol is the main constituent of sesame seed oil and is obtained from Sesamum indicum. Oral squamous cell carcinoma (OSCC) is one of the most common neoplasms affecting the oral cavity. In this study, we investigated the cytotoxic potentials of sesamol on human oral squamous carcinoma (SCC-25) cells. Human oral squamous carcinoma cells were treated with different concentrations (62.5, 125, and 250 μM/mL) of sesamol for 24 h. Cytotoxicity was analyzed by 3- (4, 5- dimethylthiazol -2- yl) -2, 5-diphenyltetrazolium bromide (MTT) assay. Intracellular reactive oxygen species (ROS) expression was investigated by dichloro-dihydro-fluorescein diacetate assay. Apoptosis-related morphology was analyzed by acridine orange/ethidium bromide staining. Caspase-9 expression was analyzed by confocal microscopic double immunofluorescence staining. Mitochondrial apoptosis-related markers are analyzed using qPCR. Sesamol treatment caused a significant cytotoxic effect in OSCC cells. Sesamol-induced cytotoxic effect was associated with intracellular ROS generation. Sesamol treatments induced a significant increase in the early and late apoptotic cells. This treatment also induced caspase-9 expression in OSCC cells. Sesamol treatments caused downregulation of Harvey rat sarcoma viral oncogene homolog (HRAS) expression at protein and gene levels. Sesamol treatment modulates intrinsic apoptotic marker gene expression in OSCC cells. Overall results confirm the anti-cancer potential of sesamol and it seems to be a promising candidate for OSCC. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma is the second most common cause of cancer death in the world and its incidence has dramatically increased worldwide in the past two decades. Syringic acid (SA) has been studied for its hepatoprotective, anti-inflammatory, immunomodulatory, free radical scavenging, and antioxidant activities. We aimed to evaluate the cytotoxic effect of SA against human hepatoma HepG2 cell line. Cytotoxicity was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. HepG2 cells were treated with SA at concentration ranges of 25, 50, and 100 µM for 24 h. Reactive oxygen species (ROS) expression was investigated by dichlorofluorescein staining assay. Morphological changes of SA-treated HepG2 cells were evaluated by acridine orange (AO) and ethidium bromide (EB) dual staining. Apoptotic marker gene expressions were evaluated by qPCR. SA treatment caused significant cytotoxicity and liberation of ROS in HepG2 cells. AO and EB staining showed membrane blebbing and distortion in SA-treated cells. Apoptotic markers such as caspases 3 and 9, cytochrome c, Apaf-1, Bax, and p53 gene expressions were significantly increased upon SA treatment indicating the possibility of apoptosis induction in HepG2 cells. This treatment also caused significant downregulation of Bcl-2 gene expression. SA has a cytotoxic effect on human HepG2 cell line, and this might be a promising agent in anticancer research. [ABSTRACT FROM AUTHOR]

Prolonged zidovudine (AZT) treatment in HIV-infected and AIDS patients is shown to induce liver toxicity leading to complications. Therapeutic regimen that could encounter this adverse effect is unavailable and management of toxicity is often symptomatic or is limited to withdrawal of therapy. In the present investigation, we evaluated the alleviating properties of silibinin (SBN), a flavanolignan obtained from Silybum marianum against subacute AZT-induced hepatotoxicity and oxidative stress in rats. AZT treatment (50 mg/kg body weight (b.w.) periorally (p.o.), daily for 45 days) caused highly significant increases in alanine transaminase, alkaline phosphatase, argininosuccinic acid lyase and bilirubin in serum. Oxidative stress is shown by a highly significant increase in lipid peroxidase and total carbonyl content and decrease in catalase and protein thiols in the liver tissue. Hyperlipidaemia is indicated by highly significant increase in total lipids and free fatty acid in serum. Evaluation of liver by haematoxylin and eosin staining shows parenchymal cell enlargement, inflammatory changes and increase in sinusoidal spaces. Simultaneous treatment of SBN (100 mg/kg b.w. p.o., daily for 45 days) significantly protected the liver against hepatotoxicity, oxidative stress and hyperlipidaemia induced by AZT, and this alleviating property is attributed to hepatoprotective, membrane-stabilizing, antioxidant and free radical scavenging properties of SBN. [ABSTRACT FROM AUTHOR]