Moringa oleifera alcoholic extract protected stomach from bisphenol A-induced gastric ulcer in rats via its anti-oxidant and anti-inflammatory activities.

This study evaluated the protective potentials of Moringa oleifera leaf alcoholic extract (MOLE) against bisphenol A (BPA)-induced stomach ulceration and inflammation in rats. Control rats received olive oil. Second group administered MOLE (200 mg/kg bwt) by oral gavage. Third group was given BPA (50 mg/ kg bwt) for 4 weeks. Fourth group administrated BPA and MOLE simultaneously. Fifth group was given MOLE for 4 weeks then administered BPA and MOLE for another 4 weeks. Bisphenol A induced gastric ulceration and decreased the volume of gastric juice, prostaglandin E2 (PGE2), reduced glutathione (GSH) and interleukin 10 (IL-10) contents, superoxide dismutase (SOD) activity, and proliferating cell nuclear antigen (PCNA) protein in stomach tissues, while increased the titratable acidity, malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) contents, and caspase-3 and NF­κB proteins in stomach tissue. However, MOLE ameliorated BPA-induced gastric ulceration and significantly increased the volume of gastric juice, PGE2, GSH and IL-10 contents, SOD activity, and PCNA protein while significantly decreased titratable acidity, MDA, TNF-α and IL-6 contents, and of NF­κB and caspase-3 proteins in gastric tissue. This study indicated that MOLE protected stomach against BPA-induced gastric injury via its anti-oxidant, anti-apoptotic, and anti-inflammatory activities.

H2S releasing Sodium sulfide protects from acute stress-induced hypertension by increasing the activity of endothelial nitric oxide synthase enzyme.

Acute stress is a feature of our daily events that affects cardiovascular system and predisposes to hypertension. H2S is now considered as a vasorelaxant gasotransmitter although it was considered as a toxic agent. In present work we studied the effect of H2S releasing Na2S in acute stress induced hypertension and cardiac damage. Rats were divided into five groups: control, Na2S, acute stress, half dose of Na2S (6 mg/kg), and finally full dose of Na2S (12 mg/kg) to acute stressed rats. BP was measured then blood samples were taken for estimation of cortisol, cardiac enzymes markers, IL-6 and H2S. Finally, animals were sacrificed, hearts and thoracic aortae were excised for histological assessment, estimation of MDA, SOD and RNA extraction of CSE. Acute stress significantly elevated BP, cortisol, cardiac enzymes markers, IL-6, and tissue levels of MDA. It also, induced cardiac cell damage with congested B.V., extravasation of blood and decreased eNOs. Moreover, acute stress reduced H2S levels, RNA expression of CSE and SOD in cardiac tissues. Na2S significantly decreased BP, serum levels of cortisol, cardiac enzymes markers, IL-6, and tissue levels of MDA. Also, Na2S elevated serum H2S, RNA expression of CSE, SOD in cardiac tissue and increased eNOs activity.