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.

Neuroprotective Potential of Allium sativum against Monosodium Glutamate-Induced Excitotoxicity: Impact on Short-Term Memory, Gliosis, and Oxidative Stress.

This study evaluated the neuroprotective potential of Allium sativum against monosodium glutamate (MSG)-induced neurotoxicity with respect to its impact on short-term memory in rats. Forty male Wistar albino rats were assigned into four groups. The control group received distilled water. The second group was administered Allium sativum powder (200 mg/kg of body weight) orally for 7 successive days, then was left without treatment until the 30th day. The third group was injected intraperitoneally with MSG (4 g/kg of body weight) for 7 successive days, then left without treatment until the 30th day. The fourth group was injected with MSG in the same manner as the third group and was treated with Allium sativum powder in the same manner as the second group, simultaneously. Phytochemical analysis of Allium sativum powder identified the presence of diallyl disulphide, carvone, diallyl trisulfide, and allyl tetrasulfide. MSG-induced excitotoxicity and cognitive deficit were represented by decreased distance moved and taking a long time to start moving from the center in the open field, as well as lack of curiosity in investigating the novel object and novel arm. Moreover, MSG altered hippocampus structure and increased MDA concentration and protein expression of glial fibrillary acidic protein (GFAP), calretinin, and caspase-3, whereas it decreased superoxide dismutase (SOD) activity and protein expression of Ki-67 in brain tissue. However, Allium sativum powder prevented MSG-induced neurotoxicity and improved short-term memory through enhancing antioxidant activity and reducing lipid peroxidation. In addition, it decreased protein expression of GFAP, calretinin, and caspase-3 and increased protein expression of Ki-67 in brain tissues and retained brain tissue architecture. This study indicated that Allium sativum powder ameliorated MSG-induced neurotoxicity through preventing oxidative stress-induced gliosis and apoptosis of brain tissue in rats.