Effect of green tea and nicotine on haematological and biochemical parameters and histopathology of bone marrow and spleen on albino rats.

We investigate the effects of green tea extract (GTE) on the attenuation of nicotine hematotoxicity, oxidative stress, inflammation and spleen and bone marrow structural lesions. Rats were treated by injecting nicotine (1,5mg/kg b.w. for 7 weeks) intraperitoneally and thereby supplementing GTE 2% orally to them. Haematological profiles, inflammation markers, neutrophil/lymphocyte (NLR), platelet/lymphocyte (PLR) and mean platelet volume (MPV/Plat) ratios- and erythrocyte sedimentation rate (ESR) were evaluated. Splenic levels of malondialdehyde (MDA), nitric oxide (NO), advanced protein oxidation products (AOPP) and catalase activity were measured. Femur bone and spleen were subjected to histological study. Nicotine-induced haematological abnormalities, a rise in the NLR and MPV/Plat ratios and ESR values with a drop in the PLR values compared to other experimental groups and leads to a significant increase in MDA, NO and AOPP levels-with a decrease in catalase activity compared to control groups. The bone marrow and spleen of nicotine exposed rats showed severe degenerative changes. GTE supplementation attenuates hematotoxicity, induce a decrease in the inflammation markers values, improved the levels of MDA, NO, AOPP and catalase activity and attenuate the adverse histological effects. GTE rich on polyphenols and flavonoids revealed by the in vitro study protects against the hazardous effects of nicotine.

GREEN TEA BEVERAGE AND EPIGALLOCATECIHIN GALLATE ATTENUATE NICOTINE CARDIOCYTOTOXICITY IN RAT.

Nicotine, the principal alkaloid in tobacco, induces a cellular damage on heart and cardiomyocyte culture. We investigate the protective role of green tea extract (GTE) against nicotine. Male albino rats were treated by injecting nicotine (1 mg/kg b.w. for 2 months) subcutaneously and thereby supplementing GTE 2% orally to them. The levels of plasma lipids, cardiac MDA (malondialdehyde) and catalase activity Mitogen-activated proteins kinases MAPKs were measured. The expression levels of (ERK 1/2, extracellular signal - regulated kinase 1/2 and P38 MAP kinase), endoplasmic reticulum stress (ERS)-related protein (GRP78 glucose regulated protein-78, HSP70 heat shock protein-70, CHOP C/EBP homologous protein), AIF (apoptosis-inducing factor) and VDAC (voltage-dependant anion channel) were evaluated by Western blot. In the in vitro study, the cardiomyocytes were exposed to nicotine (10 µM) and major GTE polyphenol epigallocatechin gallate EGCG (50 µM). Data showed that nicotine induced a significant increase on MDA levels, LDH (lactate dehy- drogenase) and aminotransferase activity compared with control. The heart sections of nicotine exposed-rats showed severe degenerative changes. Nicotine increased the expression of P38, but not ERK 1/2, ER stress-related proteins and AIF with no changes of VDAC. Concomitant GTE treatment significantly normalized and/or improved,the levels of MDA, enzymatic activity and histological injuries. The proteins expression was attenuated by GTE co-administration without any changes for VDAC. ERK 1/2 expression enhanced in GTE- treated groups. Exposure of cardiac cells to nicotine induced the expression of ERS markers and p38; the ERK 1/2 was highly expressed only in the presence of EGCG. It was suggested that green tea beverage can protect against nicotine toxicity by attenuating oxidative stress, endoplasmic reticulum stress and apoptosis. Otherwise, our results have showed that ERK1/2 and p38 are survival signaling pathways activated by GTE and EGCG.