tawab, A. A. E. M., N. N. Shahin, and M. M. AbdelMohsen, "Protective effect of Satureja montana extract on cyclophosphamide-induced testicular injury in rats", Chemico-Biological Interactions, vol. 224, pp. 196-205, 2014. Abstract

The present study investigated the protective effect of Satureja montana extract against cyclophosphamide-
induced testicular injury in rats. Total phenolic and flavonoid contents of the extract were 1.03%
and 0.34% w/w of dry herb expressed as chlorogenic acid and quercetin, respectively. HPLC analysis identified
caffeic, syringic and rosmarinic acids as the chief phenolic acids, and rutin as the major flavonoid in
the extract. Oral daily administration of S. montana extract (50 mg/kg/day) for 7 days before and 7 days
after an intraperitoneal injection of cyclophosphamide (200 mg/kg) restored the reduced relative testicular
weight, serum testosterone level and testicular alkaline phosphatase activity, raised the lowered testicular
sorbitol dehydrogenase and acid phosphatase activities, and decreased the elevated testicular
hemoglobin absorbance. It also attenuated lipid peroxidation, restored the lowered glutathione content,
glucose-6-phosphate dehydrogenase, glutathione peroxidase and glutathione reductase activities, and
improved total antioxidant capacity. Moreover, S. montana extract mitigated testicular DNA fragmentation,
decreased the elevated Fas and Bax gene expression, up-regulated the decreased Bcl-2 and peroxisome
proliferator-activated receptor-gamma (PPAR-c) gene expression and normalized Akt1 protein
level. Histopathological investigation confirmed the protective effects of the extract. Conclusively, S. montana
extract protects the rat testis against cyclophosphamide-induced damage via anti-oxidative and
anti-apoptotic mechanisms that seem to be mediated, at least in part, by PPAR-c and Akt1 up-regulation.
 2014 Elsevier Ireland Ltd. All rights reserved.

Motawi, T. K., H. A. Darwish, and A. A. E. M. tawab, "The relative efficacy of aminoguanidine and pentoxifylline in modulating endotoxin-induced cardiac stress", cell biochemistry and function , vol. 29, pp. 694–702., 2011. Abstractthe_relative_efficacy_of_aminoguanidine_.pdf

This study investigates the effect of aminoguanidine (AG), a selective inducible nitric oxide synthase (iNOS) inhibitor, and pentoxifylline (PTX), a tumour necrosis factor–alpha (TNF-a) inhibitor, on lipopolysaccharide (LPS)-induced cardiac stress. Rats were divided into four groups: group I served as a control, group II (LPS) received a single intraperitoneal injection of LPS (10mgkg–1), group III (LPS+AG) and group IV (LPS+PTX) were injected with either AG (100mgkg–1) or PTX (150mgkg–1) intraperitoneally 10days prior to LPS admin- istration. Normalization of cardiac levels of nitrite/nitrate (NOX), malondialdehyde (MDA), glutathione (GSH), heme oxygenase-1 (HO-1), glutathione peroxidase (GPx) and Na+,K +-ATPase activities was evident in the AG group. Both AG and PTX decreased the elevated serum TNF-a levels, the activities of lactate dehydrogenase (LDH), creatine kinase (CK) and cardiac myeloperoxidase (MPO). The levels of adenosine triphosphate (ATP), adenosine diphosphate (ADP) and phosphocreatine (PCr) were enhanced following AG and PTX pretreat- ments. Calcium (Ca2+) levels were altered, and the histopathological observations supported the described results. Conclusively, the study highlights the cardioprotective potential of AG and PTX with superior results from AG. These findings reveal the relative contribution of nitric oxide and TNF-a to oxidative stress and energy failure during endotoxemia.

Motawi, T. K., H. A. Darwish, and A. A. E. M. tawab, "Effects of Caffeic Acid Phenethyl Ester on Endotoxin-Induced Cardiac Stress in Rats: A Possible Mechanism of Protection ", J BIOCHEM MOLECULAR TOXICOLOGY, vol. 25, issue 2, pp. 84-94, 2011. Abstractcape_and_endotoxin_cardiac_stress.pdf

Endotoxins (lipopolysaccharides; LPS) are known to cause multiple organ failure, including myocardialdysfunction.Thepresentstudyaimedtoin- vestigatethemechanismofcaffeicacidphenethylester (CAPE) protection against LPS-induced cardiac stress. Rats were allocated into three groups; group 1 served as a normal control group, group 2 (LPS) received a single intraperitoneal injection of LPS (10 mg/kg), group 3 (LPS + CAPE) was injected intraperitoneally with CAPE (10 mg/kg/day; solubilized in saline con- taining 20% tween 20) throughout a period of 10 days prior to LPS injection. Rats were maintained 4 h be- fore sacrifice. Caffeic acid phenethyl ester pretreat- mentnormalizedLPS-enhancedactivitiesofserumcre- atine kinase (CK) and lactate dehydrogenase (LDH) as well as glutathione peroxidase (GPx), and myeloper- oxidase (MPO) in cardiac tissue. A significant reduc- tion of the elevated levels of serum tumor necro- sis factor-alpha (TNF-α) as well as serum and car- diac nitrite/nitrate (NOx) was achieved after CAPE pretreatment. CAPE also restored malondialdelyde (MDA), reduced glutathione (GSH), and cytosolic calcium (Ca2+) levels in the heart. A marked in- duction of cardiac heme oxygenase-1 (HO-1) pro- tein level was detected in CAPE-pretreated group. Whereas,LPS-inducedreductionofadenosinetriphos- phate (ATP) and phosphocreatine (PCr) levels was insignificantly changed. Conclusively, the early treat- ment with CAPE maintained antioxidant defences, re- duced oxidative injury, cytokine damage, and inflam- mation but did not markedly improve energy sta- tus in cardiac tissue. The beneficial effect of CAPE might be mediated, at least in part, by the superinduc- tion of HO-1.

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