The investigation of the effects of cinnamomum cassia extracts on TYPE 1 diabetes in vitro model

There are a large number of studies suggesting that increased oxidative stress plays a pivotal role in the development of complications of diabetes in patients with Type 1 diabetes mellitus (T1DM). It is alleged that increased oxidative stress induces oxidative DNA damage and that it may contribute the development of cancer due to insufficient DNA repair capacity. Therefore, studies focused on investigation of the protective drugs and herbal products against to oxidative stress and DNA damage in diabetic patients. Cinnamon is a herbal product that its diverse biological activities including antidiabetic and anti-tumor properties has been proved by scientific studies. In recent years, it is particularly used by diabetic patients in the form of tea and food supplement in an attempt to decrease insulin resistance and regulate blood glucose and lipid levels. Cinnamomum cassia (C. cassia) is a cinnamon species commonly presents in commercial cinnamon preparations. The purposes of our study were; 1- To investigate the effects of C. cassia bark extracts on cell viability and the apoptotic activities of the extracts on type 1 diabetes in vitro model; 2- To investigate of the effects of the extract(s) with no apoptotic activity on endogenous and H2O2-induced oxidative DNA damage; 3- To investigate the implication of reactive oxygen species (ROS) generation on these effects. In the present study, IC50 values of the extracts were determined by WST-1 test. Annexin V/PI and TUNEL tests were performed for determination of apoptotic activities, by using flow cytometry. The effects of butanol and water extracts with non-apoptotic activities on endogenous and H2O2-induced oxidative DNA damage were determined by alkali comet assay and confirmed by TUNEL test. The effects on the production of ROS were investigated by DCF-DA test using flow cytometry. Our results showed that the C. cassia water extract has protective effect against to H2O2-induced oxidative DNA damage and that this effect might be related to its reducing effect on ROS production in T1DM in vitro cell model.