Gingerol fractions bioactivity against butanone cytotoxicity induced in newborns of mice.

OBJECTIVE: Accumulating studies have demonstrated the potential activity of ginger in treating and managing several diseases but little is known about its protective effects against teratogenicity of chemical toxins. Thus, in this study, we have evaluated the protective effect of gingerol fraction (GF) against methyl ethyl ketone (MEK) induced teratogenic effects in newborns of mice. MATERIALS AND METHODS: A total of 30 mature females and fifteen male mice (Mus musculus) weighing 25-30 g were included in this study. The pregnant mice were divided into three groups (10 mice each); control group (GI, mice received normal drinking water; NDW), methyl ethyl ketone (MEK) treated group (GII, received MEK at a dose of 350 mg/kg body weight in NDW), and GF treated group (GIII; mice received GF at a dose of 25 mg/kg in NDR). Histological analysis, cellular oxidative, and antioxidant enzymes, fibrosis, and apoptosis of brain, liver, and kidney tissues were estimated by histological and immunoassay techniques. RESULTS: In this study, the treatment of pregnant female mice with gingerol fractions (GF) at a dose of 25 mg/kg significantly protected all tissues organs of mothers and their offspring against the teratogenic effects induced by MEK at a dose of 350 mg/kg. A significant improvement in cellular antioxidant enzymes GSH, SOD, and peroxidase activities along with a reduction in the initiation of cellular oxidative free radicals (TBARS) was reported in GF treated mice compared to mice intoxicated with MEK (350 mg/kg). In addition, a significant reduction in cellular fibrosis and apoptosis was reported in all tissues of mothers and their offspring's following treatment with GF. HPLC analysis of ginger extracts estimated a set of polyphenolic compounds such [6]-gingerol, [8]-gingerol, [10]-gingerol, and [6]-shogaol which are responsible for the antioxidant, anti-fibrotic, and anti-apoptotic protective effects against teratogenic effects of MEK. CONCLUSIONS: Gingerol fractions (GF) at a dose of 25 mg/kg significantly protected all tissues organs of mothers and their offspring against the teratogenic effects induced by MEK at a dose of 350 mg/kg. The beneficial effects of ginger phenolic compounds; [6]-gingerol, [8]-gingerol, [10]-gingerol, and [6]-shogaol against teratogenic effects of MEK proceeded through their antioxidant, anti-fibrotic, and anti-apoptotic properties.

Quercetin protects against experimentally-induced myocardial infarction in rats by an antioxidant potential and concomitant activation of signal transducer and activator of transcription 3.

This study tested if the protective effect of quercetin (QUR) against experimentally-induced acute myocardial infarction (AMI) in rats involves modulating the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway. Rats were divided into 6 groups as sham-operated (control), control + QUR, AMI, AMI + QUR, AMI + S3I-210 (a STAT3 inhibitor), and AMI + QUR + S31-201. QUR (50 mg/kg/orally) and S3I-201 (a STAT3 inhibitor) (5 mg/kg/i.p.) were administered for 7 days before the induction of AMI and the experiment was ended 24 h post-AMI. Pre-treatment with QUR reduced the infarct size, improved the left ventricular (LV) functions and the structure of the myofibrils and the mitochondria, and reduced circulatory levels of lactate dehydrogenase (LDH), creatinine-kinase MB (CKMB), and troponin-I. QUR also reduced LV levels of reactive oxygen species (ROS) and malondialdehyde (MDA), inhibited the opening of the mitochondria transition pores (mtPTP), and reduced protein levels of cytochrome-C, cleaved caspase-3 and p-JAK2 (Tyr1007/1008) in the LVs of AMI rats. In the LV of both the control and AMI rats, QUR didn't affect the levels of p-JAK2 but significantly increased the levels of total glutathione (GSH) and manganese superoxide dismutase (MnSOD), reduced the levels of Bax and the nuclear levels and activity of NF-κB p65, tumor necrosis-factors-α (TNF-α), interleukin-6 (IL-6), and p-STAT1 (Ser727) but further increased the levels of p-STAT3 (Ser727). All these effects exerted by QUR were partially reversed but the decrease in nuclear protein levels and activity of NFκB, levels of TNF-α and IL-6, and pSTAT3 were completely prevented by co-administration of S3I-201. In conclusion, QUR protects against MI by upregulation of antioxidants and activation of STAT3.