H.S., S., T. M.M, E. A, A. T., and H. I., "Combination of Caffeine and Liver Albumin Plus Protects against Smoking-Induced Liver Injury in Rats", Dubai Medical Journal, 2018.
Shoukry, H. S., R. A. D. W. A. T. HASSANIEN, R. A. Rasheed, M. O. A. T. A. Z. M. KAMEL, E. R. Ibrahim, and H. A. L. A. S. IBRAHIM, "Vitamin E Improves Doxorubicin Induced Nephrotoxicity; Possible Underlying Mechanisms", Medical journal of Cairo University , vol. Vol. 86,, 2018.
Hamzawy, M., S. A. A. Gouda, L. rashid, M. A. Morcos, H. shoukry, and N. Sharawy, "The cellular selection between apoptosis and autophagy: roles of vitamin D, glucose and immune response in diabetic nephropathy.", Endocrine, vol. 58, issue 1, pp. 66-80, 2017 Oct. Abstract

BACKGROUND AND AIMS: Apoptosis, autophagy and cell cycle arrest are cellular responses to injury which are supposed to play fundamental roles in initiation and progression of diabetic nephropathy (DN). The aims of the present study is to shed light on the potential effects of vitamin D analog 22-oxacalcitriol (OCT) on different cell responses during DN, and the possible interplay between both glucose, immune system and vitamin D in determining the cell fate.

METHOD: All rats were randomly allocated into one of three groups: control, vehicle-treated DN group and OCT-treated DN group. Eight weeks after induction of diabetes, the rats were killed. Fasting blood glucose levels, serum 25 (OH) D, renal functions, cytokines and gene expression of autophagy, apoptotic and cell cycle arrest markers were assessed. In addition, the histological assessment of renal architecture was done.

RESULTS: OCT treatment remarkably improved the renal functions and albuminuria. The reductions in mesangial cell hypertrophy, extracellular matrix as well as cell loss were significantly associated with upregulation of pro-autophagy gene expressions and downregulation of both pro-apoptotic and G1-cell cycle arrest genes expression. The reno-protective effects of OCT treatment were associated with significant attenuation of the fasting blood glucose, serum IL-6, renal TLR-4 and IFN-g gene expression.

CONCLUSION: Modulator effects of OCT on glucose and immune system play important roles in renal cell fate decision and chronic kidney disease progression.

Hamzawy, M., S. A. A. Gouda, L. Rashed, M. A. Morcos, H. shoukry, and N. Sharawy, "22-oxacalcitriol prevents acute kidney injury via inhibition of apoptosis and enhancement of autophagy.", Clinical and experimental nephrology, vol. 23, issue 1, pp. 43-55, 2019 Jan. Abstract

BACKGROUND: The pathophysiology of ischemic acute kidney injury (AKI) is thought to include a complex interplay between tubular cell damage and regeneration. Several lines of evidences suggest a potential renoprotective effect of vitamin D. In this study, we investigated the effect of 22-oxacalcitriol (OCT), a synthetic vitamin D analogue, on renal fate in a rat model of ischemia reperfusion injury (IRI) induced acute kidney injury (AKI).

METHODS: 22-oxacalcitriol (OCT) was administered via intraperitoneal (IP) injection before ischemia, and continued after IRI that was performed through bilateral clamping of the renal pedicles. 96 h after reperfusion, rats were sacrificed for the evaluation of autophagy, apoptosis, and cell cycle arrest. Additionally, assessments of toll-like receptors (TLR), interferon gamma (IFN-g) and sodium-hydrogen exchanger-1 (NHE-1) were also performed to examine their relations to OCT-mediated cell response.

RESULTS: Treatment with OCT-attenuated functional deterioration and histological damage in IRI induced AKI, and significantly decreased cell apoptosis and fibrosis. In comparison with IRI rats, OCT + IRI rats manifested a significant exacerbation of autophagy as well as reduced cell cycle arrest. Moreover, the administration of OCT decreased IRI-induced upregulation of TLR4, IFN-g and NHE-1.

CONCLUSION: These results demonstrate that treatment with OCT has a renoprotective effect in ischemic AKI, possibly by suppressing cell loss. Changes in the expression of IFN-g and NHE-1 could partially link OCT to the cell survival-promoted effects.

Mubarak, H. A., M. M. Mahmoud, H. S. Shoukry, D. H. Merzeban, S. S. Sayed, and L. A. Rashed, "Protective effects of melatonin and glucagon‐like peptide‐1 receptor agonist (liraglutide) on gastric ischaemia–reperfusion injury in high‐fat/sucrose‐fed rats", Clin Exp Pharmacol Physiol., 1975 Dec, 2018. Abstract

We have recently shown that 5% CO2/95% O2 in the serosal bathing solution, with 100% O2 in the mucosal solution, results in CO2-diffusion limitation of acid secretion in bullfrog gastric mucosa. Changing to 10% CO2/90% 02 on both surfaces doubles the acid secretory rate. We calculate that, were the rate of oxygen consumption to increase significantly as a result of secretory stimulation, the tissue would now be oxygen limited. This prediction is tested by raising the P02 by increasing the total pressure in a hyperbaric chamber. Since no change in acid secretory rate or potential difference was observed upon changing from PO2 = 0.9 to PO2 = 1.9 atm, we conclude that the tissue is not O2 limited at normal pressure. Decreasing PO2 below 0.9 atm, by contrast, decreases the acid secretory rate and raises both PD and resistance. We infer that the rate of oxygen consumption did not rise significantly when acid secretion was increased by supplying sufficient CO2.

Sabry, M. M., M. M. Mahmoud, H. S. Shoukry, L. Rashed, S. S. Kamar, and M. M. Ahmed, "Interactive effects of apelin, renin-angiotensin system and nitric oxide in treatment of obesity-induced type 2 diabetes mellitus in male albino rats.", Archives of physiology and biochemistry, pp. 1-11, 2018 Mar 22. Abstract

Apelin and its receptor (APJ) are involved in the regulation of a variety of pathophysiological processes. We studied the effect of apelin treatment on obesity-induced type 2 diabetes mellitus (T2DM) and possible interaction between apelin/APJ system and renin-angiotensin system (RAS). Forty eight male albino rats were divided into two groups: control group and diabetic group. Diabetic group was subdivided into: control diabetic, apelin-treated, apelin + losartan-treated, apelin + l-NAME-treated and losartan-treated diabetic subgroup. Administration of apelin-13 yielded an improvement of IR, dyslipidaemia, inflammation, oxidative stress with significant decrease in AT1R gene expression and significant increase in ACE2 gene expression in adipose tissues. Losartan + apelin yielded a further significant decrease in ATR1 gene expression, glycaemic indices, serum TGs and TPA versus Apelin only. Adding l-NAME in subgroup (2D) reversed the effect of apelin. We suggested that the beneficial effect of Apelin is mainly mediated by NO-activated pathway and/or ACE2/Ang (1-7) dependent pathway.

ElHamzawy, P. D. M., P. D. H. Shawky, D. H. Shoukry, and P. D. L. Rashed, Contribution of Oxytocin and Testosterone in attenuating atherosclerosis and adipose tissue inflammation in male rats, , 2012.
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