Basic Informations

C.V

I. PERSONAL INFORMATION:

NAME:  Heba Mohsen Mahmoud Taha.

BIRTH DATE:  31/01/1985.

NATHIONALITY:  EGYPTIAN.

RELIGION: MUSLIM.

ADDRESS: ELSHOBAN ELMOSLIMIN STREET, BENI-SUEF, EGYPT.

TELEPHONE NUMBER: 01118223302 (MOBILE) – 0822316644 (HOME)

E-MAIL: hebaaldaw@yahoo.com

MARITAL STATUS: MARRIED

II. Education:

• B. Ph. Sc., (Bachelor Degree in Pharmaceutical Sciences), Excellent, Faculty of Pharmacy, Beni-Suef University, Egypt, 2006.

·MS.D, (Master degree in Pharmacology and Toxicology), 2014.

  III.  Employment history:

• Demonestrator of Pharmacology & Toxicology, Faculty of Pharmacy, Beni-Suef University (2006-2014)         

 • Assistant Lecturer of Pharmacology & Toxicology, Faculty of Pharmacy, Beni-Suef University (2014 till now).

 IV. TRAINING COURSES:

    • General English at American University in Cairo (AUC).

·        ICDL at Beni-Suef University.           

Master Title

Pharmacological study of the effects of certain chelating agents and some hypocholesterolemic drugs in hypercholesterolemic rats

Master Abstract

In the present study, the effects of simvastatin, CaNa2EDTA, DMSA and vitamin E were investigated on several parameters related to hypercholesterolemia. Hypercholesterolemia was induced by feeding rats with cholesterol-rich diet for six weeks. All drugs were given concomitantly with cholesterol-rich diet for six weeks. The effects of the test drugs and their combinations on lipid profile markers including serum total cholesterol (TC), triglycerides (TG), low density lipoproteins cholesterol (LDL-c), very low density lipoproteins cholesterol (VLDL-c) and high density lipoproteins cholesterol (HDL-c) were estimated. Also their effects on some oxidative stress markers including serum malondialdehyde (MDA), blood superoxide dismutase (SOD) and reduced glutathione (GSH) as well as serum total nitrate/nitrite (NOx), aortic endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) were determined. Furthermore, aortic calcium and wall thickness as well as serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), urea, creatinine and glucose were determined. In addition, the effects of the test drugs on body weight gain were estimated. The main findings of the current study could be summarized as follows: 1. Diet-induced hypercholesterolemia resulted in alterations in the lipid profile, a state of oxidative stress and hyperglycemia coupled by decreased body weight gain and compensatory increase in serum NOx level of rats. 2. In addition, decreased aortic eNOS activity as well as increased aortic iNOS activity, calcium content and wall thickness were observed. 3. Simvastatin, CaNa2EDTA, DMSA and vitamin E significantly reduced serum TC, TG and VLDL-c levels of hypercholesterolemic rats. 4. Simvastatin and DMSA significantly reduced serum LDL-c level while CaNa2EDTA and vitamin E did not significantly affect serum LDL-c level of hypercholesterolemic rats. 5. DMSA significantly increased serum HDL-c level of hypercholesterolemic rats while simvastatin, CaNa2EDTA and vitamin E did not significantly affect it. 6. Simvastatin, CaNa2EDTA, DMSA and vitamin E significantly decreased atherogenic index of hypercholesterolemic rats. 7. DMSA significantly increased high density lipoproteins cholesterol/total cholesterol ratio (HTR) of hypercholesterolemic rats while simvastatin, CaNa2EDTA and vitamin E did not significantly change it. 8. No interaction was observed between simvastatin and CaNa2EDTA, DMSA or vitamin E on serum TC or LDL-c levels when given concomitantly. 9. There was an additive interaction between simvastatin and CaNa2EDTA or vitamin E on serum TG and VLDL-c as well as serum HDL- c levels when co-administered together. 10. No interaction was observed between simvastatin and DMSA on serum TG level while an additive interaction was observed between them on serum VLDL-c and HDL-c levels when combined together. 11. No interaction was observed between simvastatin and CaNa2EDTA, DMSA or vitamin E on atherogenic index while an additive interaction was observed between simvastatin and the other drugs on HTR when co-administered together. 12. Simvastatin, CaNa2EDTA, DMSA and vitamin E significantly decreased serum MDA level while increasing blood GSH level of hypercholesterolemic rats. 13. CaNa2EDTA, DMSA and vitamin E significantly elevated blood SOD activity of hypercholesterolemic rats while simvastatin did not significantly affect it. 14. An additive interaction was observed by concurrent administration of simvastatin with CaNa2EDTA or vitamin E on serum MDA and blood GSH levels. 15. A potentiating effect was observed between simvastatin and CaNa2EDTA or vitamin E on blood SOD activity when combined together. 16. No interaction was observed between simvastatin and DMSA on serum MDA level or blood SOD activity; whereas there was an additive interaction between them on blood GSH level when co-administered together. 17. Simvastatin significantly increased serum NOx level of hypercholesterolemic rats. 18. CaNa2EDTA, DMSA and vitamin E did not significantly change serum NOx level of hypercholesterolemic rats. 19. Simvastatin, CaNa2EDTA, DMSA and vitamin E significantly increased aortic eNOS activity while decreasing aortic iNOS activity, calcium content and wall thickness of hypercholesterolemic rats. 20. No interaction was observed between simvastatin and CaNa2EDTA, DMSA or vitamin E on serum NOx level, aortic eNOS and iNOS activities, calcium content or wall thickness when given concomitantly. 21. CaNa2EDTA and vitamin E significantly lowered serum glucose level of hypercholesterolemic rats; whereas simvastatin and DMSA did not significantly affect it. 22. A potentiating effect was observed between simvastatin and CaNa2EDTA on serum glucose level when co-administered together. 23. Simvastatin, CaNa2EDTA, DMSA and vitamin E did not significantly affect body weight gain of hypercholesterolemic rats. According to the previous findings, it could be concluded that: • Feeding rats with cholesterol-rich diet for six weeks caused hypercholesterolemia associated with oxidative stress. • Treatment of hypercholesterolemic rats with simvastatin, CaNa2EDTA, DMSA or vitamin E as well as their combinations markedly improved hypercholesterolemia and its associated oxidative stress. • The hypolipidemic actions of CaNa2EDTA, DMSA and vitamin E are probably due to their antioxidant properties. • Simvastatin, CaNa2EDTA, DMSA and vitamin E improved endothelial function by increasing aortic eNOS and decreasing aortic calcification and wall thickening. • Chelating agents such as CaNa2EDTA and DMSA could be used in the treatment of some cardiovascular diseases associated with hypercholesterolemia by removing lipid/calcium plaque from blood vessels. • Further clinical trials are needed to support the previous findings.

PHD Title

Pharmacological study of the possible protective effects of certain antioxidants and some vasodilators against paracetamol-induced hepatotoxicity in rats

PHD Abstract

In the present study, the protective effects of NAC, naringenin, vanillin and carvedilol were investigated on several parameters related to paracetamol-induced hepatotoxicity in rats. Hepatotoxicity was induced by a single oral dose of paracetamol (1 g/kg). All drugs were given for 7 successive days before paracetamol-administration. The effects of the tested drugs on hepatotoxicity markers including serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and gamma-glutamyl transferase (GGT) activities as well as serum total protein (TP) level were estimated. Also their effects on oxidative and nitrosative stress markers including hepatic malondialdehyde (MDA), reduced glutathione (GSH), catalase and total nitrate/nitrite (NOx) contents or activity were assessed. In addition, the effects of the tested drugs on serum tumor necrosis factor-alpha (TNF-a) and interleukin-1ß (IL-1ß) levels were also determined as inflammatory markers. Histopathological examination of liver tissues was also done. Moreover, immunohistochemical study and western blot analysis were done for estimation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression levels in liver tissues. Furthermore, the effects of the test drugs on the relative liver weight were determined. The main findings of the current study could be summarized as follows: 1. Paracetamol-induced hepatotoxicity significantly elevated serum ALT, AST, LDH and GGT activities and significantly decreased serum TP level. 2. N-acetyl cysteine significantly decreased serum ALT, AST, LDH and GGT activities while it did not significantly affect serum TP level of hepatotoxic rats. 3. Naringenin significantly reduced serum ALT, AST, LDH and GGT activities and significantly elevated serum TP level. 4. Vanillin significantly decreased serum ALT, AST and GGT activities and significantly increased serum TP level. It did not significantly affect serum LDH activity of hepatotoxic rats. 5. Carvedilol significantly decreased serum ALT and AST activities and significantly increased serum TP level. It did not significantly change serum LDH and GGT activities of hepatotoxic rats. 6. Paracetamol-induced hepatotoxicity significantly increased hepatic MDA, catalase and NOx contents or activity while it significantly decreased hepatic GSH content. 7. N-acetyl cysteine significantly decreased hepatic MDA content while it significantly increased hepatic GSH and NOx contents. 8. Naringenin significantly decreased hepatic MDA content and catalase activity while it significantly increased hepatic GSH content. It did not significantly affect hepatic NOx content of hepatotoxic rats. 9. Vanillin significantly reduced hepatic MDA content and catalase activity while it significantly increased hepatic GSH and NOx contents. 10. Carvedilol significantly reduced hepatic MDA content and catalase activity while it did not significantly change hepatic GSH and NOx contents of hepatotoxic rats. 11. Neither paracetamol nor the test drugs significantly affect the relative liver weight. 12. Paracetamol-induced hepatotoxicity resulted in significant elevation of serum TNF-a and IL-1ß levels. 13. N-acetyl cysteine, naringenin, vanillin and carvedilol significantly decreased paracetamol-induced elevation of serum TNF-a and IL-1ß levels. 14. Induction of hepatotoxicity by paracetamol significantly increased hepatic iNOS and COX-2 expressions. 15. N-acetyl cysteine, naringenin, vanillin and carvedilol significantly reduced hepatic iNOS and COX-2 expressions. 16. Western blot analysis of liver tissues of paracetamol-treated rats revealed significant increase in hepatic iNOS and COX-2 expression levels compared to normal control group. 17. N-acetyl cysteine, naringenin, vanillin and carvedilol reduced paracetamol-induced elevation in hepatic iNOS and COX-2 expression levels. 18. Histopathological examination of liver tissues of paracetamol-treated rats showed severe hepatic damage manifested by moderate vascular congestion of central vein and hepatic sinusoids, moderate inflammatory changes, inflammatory cell infiltration, fatty degeneration of hepatocytes, centrilobular necrosis and hyperplasia of Kupffer cells. 19. Histopathological examination of liver tissues of rats treated with NAC, naringenin, vanillin and carvedilol showed mild hepatic changes than those observed in paracetamol group indicating that they began to restore the normal appearance and physiological state of liver tissues. According to the previous findings, it could be concluded that: • Paracetamol-induced hepatotoxicity resulted in hepatic dysfunction and a state of oxidative stress. • Paracetamol also induces inflammation as evidenced by increased serum levels of TNF-a and IL-1ß as well as hepatic iNOS and COX-2 expressions. • In addition, hepatic cellular injury and inflammatory changes were observed in liver tissues. • Prophylactic administration of NAC, naringenin, vanillin and carvedilol to hepatotoxic rats attenuated most of the biochemical, histopathological and immunohistochemical changes induced in rats by paracetamol. • The most likely proposed mechanism for the observed effects of the test drugs is probably related to their antioxidant properties. • In addition, these drugs also possess anti-inflammatory properties due to their ability to suppress NF-?B activation and inhibit paracetamol-induced elevation of iNOS and COX-2 expressions. • Naringenin, vanillin and carvedilol could be promising protective agents for clinical use against paracetamol-induced hepatotoxicity. • Further clinical studies are required to support the previous findings.