Cytotoxic and apoptotic potential of Myristica fragrans Houtt. (mace) extract on human oral epidermal carcinoma KB cell lines

Several studies have revealed that certain naturally occurring medicinal plants inhibit the growth of various cancers. The present study was conducted to evaluate cytotoxicity and apoptotic induction potential of Myristica fragrans Houtt mace extract. The cytotoxic activity of the Myristica fragrans Houtt mace acetone extract was assayed by MTT assay on human oral epidermal carcinoma KB cell lines. KB cells were incubated with different concentration of mace extract ranging from 25 to 125 µg/mL for 24hrs. The apoptotic induction potential was also studied by the analysis of Bcl-2 protein and gene expression in mace extract incubated KB cell lines using western blotting technique and real-time polymerase chain reaction. The mace extract exhibited cytotoxicity and anticancer effect against KB cell lines and it also suppressed the growth of cancer cells, therefore growth inhibitory effect was noted in extract treated cell lines. The apoptotic potential of mace extract was accompanied by reduced gene expression of Bcl-2 compared to the untreated KB cells. The mace extract shows the cytotoxic activity and induced the apoptosis through the modulation of its target genes Bcl-2 in the KB cell lines, suggesting the potential of mace as a candidate for oral cancer chemoprevention. This can be further investigated in vivo for its anticancer potential.

Effect of rosmarinic acid on insulin sensitivity, glyoxalase system and oxidative events in liver of fructose-fed mice

The study investigates the effects of rosmarinic acid [RA] on insulin sensitivity, protein glycation and oxidative events in fructose-fed mice, a model of insulin resistance [IR]. Experiments were performed in four groups of animals administered either fructose diet or starch diet with and without RA administration. Insulin sensitivity indices were computed at the end of the treatment period. Redox homeostasis in liver was determined by assaying lipid peroxidative markers and antioxidants in the liver. Glyoxalase system and protein damage were assessed by assaying aldehydes, glyoxalase I and II, protein carbonyls, total thiols and nitrosothiols. Protein glycation was studied by measuring glycated hemoglobin, fructosamine and advanced glycation end products. Mitochondrial function was assessed by assaying succinate dehydrogenase and calcium ATPase. Fructose administration caused glycation of proteins, changes in metabolic parameters, inactivation of the glyoxalase system and depletion of antioxidants. Oxidative stress and reduced mitochondrial function were observed. Administration of RA to fructose-fed mice mitigated the above alterations. The data suggest that metabolic and redox disturbances in this dietary model of IR could be mitigated by RA. The antioxidant action of RA could be one of the contributing mechanisms for the improvement of insulin sensitivity