The brain renin-angiotensin system (RAS) is considered a crucial regulator for physiological homeostasis and disease progression. We evaluated the protective effects of the angiotensin receptor blocker (ARB) telmisartan and the angiotensin-converting enzyme 2 (ACE2) activator xanthenone on experimental cerebral ischemia/reperfusion (I/R) injury. Rats were divided into a sham control, a cerebral I/R control, a standard treatment (nimodipine, 10 mg/kg/day, 15 days, p.o.), three telmisartan treatments (1, 3, and 10 mg/kg/day, 15 days, p.o.), and three xanthenone treatments (0.5, 1, and 2 mg/kg/day, 15 days, s.c.) groups. One hour after the last dose, all rats except the sham control group were exposed to 30-min cerebral ischemia followed by 24-h reperfusion. Brain ACE and ACE2 activities and the apoptotic marker caspase-3 levels were assessed. Glutathione (GSH), malondialdehyde (MDA), and nitric oxide end products (NOx) as oxidative markers and tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and IL-10 as immunological markers were assessed. Histopathological examination and immunohistochemical evaluation of glial fibrillary acidic protein (GFAP) were performed in cerebral cortex and hippocampus sections. Telmisartan and xanthenone in the higher doses restored MDA, NOx, TNF-α, IL-6, caspase-3, ACE, and GFAP back to normal levels and significantly increased GSH, IL-10, and ACE2 compared to I/R control values. Histopathologically, both agents showed mild degenerative changes and necrosis of neurons in cerebral cortex and hippocampus compared with I/R control group. Modulation of brain RAS, either through suppression of the classic ACE pathway or stimulation of its antagonist pathway ACE2, may be a promising strategy against cerebral I/R damage.

Liver mitochondrial RNA synthesis (as measured by an RNA polymerase assay) in adrenalectomized ovariectomized rats increased (42 %) 1 h after injection of 0.5 mg cortisol/100 g b. wt. Nuclear RNA synthesis increased (130\p=n-\171%) 4 h after injection of 4 mg cortisol/100 g but did not increase after treatment with the lower dosage of cortisol after 4 h. There was no

1. RNA was isolated from the ovarian and uterine tissues of calves by the cold phenol procedure. 10 OD of uterine-RNA, ovarian-RNA or the equivalent volume of normal saline was injected into the uterine lumen of ovariectomized mice.2. Alkaline phosphatase and \g=b\-glucuronidase levels in the uterus were studied 3 days following the intra-uterine injections.3. Results indicate that both U-RNA and O-RNA were able to induce protein (enzyme) production in the atrophied mouse uterus. Although U-RNA caused higher \g=b\-glucuronidase content of the uterus than O-RNA, the physiological state of the tissue used to supply the RNA did not have any effect. 4. Ribonuclease and KOH digestion of the RNA extract abolishes its action. Actinomycin D given simultaneously with RNA represses the latter's action.5. The possibility of hormonal contamination in the RNA extraction is discussed and should be ruled out after ether washing.Recent studies support the concept that steroid hormones act on nuclear DNA to stimulate messenger-RNA (m-RNA) synthesis (Gorski et al. 1965;Kochakian 1962). This m-RNA initiates biochemical and structural changes in the uterine cells following hormonal application (Ui & Mueller 1963). Such interpretation is substantiated by various studies on protein biosynthesis in vivo (Coster Sc Kochakian 1962; Williams-Ashman et al. 1963) and in vitro {Wilson 1962), nucleic acid fluctuation in castrate and hormone treated animals (Wicks et al. 1965; Kochakian 8c Harrison 1962), local puromycin application to oestrogen treated rats (Talwar Sc Segal 1963) and in situ injections of RNA in the uterine

RNA from tissues subjected to very high doses of 17β-oestradiol in vivo and in vitro was injected into the uteri of ovariectomized mice before and after ether washing of the RNA. Alkaline phosphatase content of the atrophied uterus was measured after the RNA injections. Results indicate that alkaline phosphatase induction is due to RNA and that ether washing completely eliminates hormonal contamination. The role played by the hormone-cytoplasm requires further attention.

In this work, we carry out the testing of some Benzimidazole derivatives as anti-inflammatory using Indomethacin 10mg/Kg, diclofenac sodium 7mg/ Kg, celecoxib 100mg/Kg and tested compounds of 200mg/Kg. The tested compounds showed anti-inflammatory activity in comparison with the standard reference drugs. In additionally, carrying out the testing of ulcer index for some testing compounds 600mg/Kg comparing with indomethacin 100mg/Kg, the testing revealed indomethacin causes ulcer in stomach of the testing animals, while the testing compounds no ulcerated the stomach of the testing animal.