faculty of Medicine

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About faculty of Medicine

The Faculty of Medicine was established in 1973, Tripoli, to contribute in qualifying medical personnel. The Faculty graduated its first batch in 1980.


It is one of the largest faculties at the University of Tripoli. It an important edifice of knowledge, so that during the past four decades this Faculty has contributed to preparing and graduating qualified doctors who had been very successful in performing their assigned role in the medical field in all the hospitals located all over the country. The graduate doctors were able to provide the best health services. The Faculty of Medicine has more than 493 faculty members, most of them are national elements who were among the first batches in this college and who contributed to providing the necessary health services in hospitals, clinics and dispensaries.


Many graduates of this Faculty have been sent to complete their studies abroad and who have proven their capabilities in scientific and clinical achievement with the testimony of many international universities. The Faculty seeks to activate graduate programs in various disciplines. It works to develop the vocabulary of its curricula and teaching methods that keep pace with the requirements of international quality.

Facts about faculty of Medicine

We are proud of what we offer to the world and the community




Academic Staff






Master's Degree
Major Family and community Medicine





Who works at the faculty of Medicine

faculty of Medicine has more than 237 academic staff members

staff photo

Dr. Mohamed A M Al Griw

الدكتور محمد عبد السلام القريو هو أحد أعضاء هيئة التدريس بقسم الأنسجة والوراثة بكلية الطب البشري. يعمل الدكتور محمد القريو بجامعة طرابلس كأستاذ مشارك منذ أغسطس 2019م، وله العديد من المنشورات العلمية في مجال تخصصه. أكثر من 18 سنة من العمل الأكاديمي والإداري مع جامعة طرابلس، ووزارة التعليم العالي والبحث العلمي، والمركز الوطني لضمان جودة واعتماد المؤسسات التعليمية والتدريبية في مجالات التخطيط الاستراتيجي، والجودة وضمانها في التعليم العالي، والاعتماد الأكاديمي، وتصنيف الجامعات. وتحصل على عدد من الشهادات في مجال التخطيط الاستراتيجي، والجودة وضمانها والاعتماد في التعليم العالي. ويعمل حالياً مع فرق عمل الهيئة الوطنية لأبحاث وتحاليل البصمة الوراثية ويُعد عضو مؤسس لبرنامج ليبيا جينوم بالهيئة - دولة ليبيا.


Some of publications in faculty of Medicine

Screening of Three Exons of PKD1 gene In Five Patients with Autosomal Polycystic Kidney Disease

Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common genetic kidney disorders with the incidence of 1 in 1,000 births. ADPKD is genetically heterogeneous with two genes identified: PKD1 (16p13.3, 46 exons) and PKD2 (4q21, 15 exons). Eighty five percent of the patients with ADPKD have at least one mutation in the PKD1 gene and fifteen percent of the patients have one mutation in PKD2 gene. Direct sequencing of one patient and his sequence of PKD1 gene demonstrated a missense mutation GCC----CCC substitution in exon 13 with cause change amino acid of Alanine to Proline at codon 1029. Three brothers have deletion mutation in exon 15, one patient missense mutation GGC---GCC in exon 19 which cause change amino acid of Glycine to Alanine at codon 2530. Molecular diagnostics of ADPKD relies on mutation screening of PKD1 and PKD2, which is complicated by extensive allelic heterogeneity and the presence of six highly homologous sequences of PKD1. PCR strategy was used to screen sequence variants with heteroduplex analysis and several affected individuals were discovered to have clusters of base pair substitutions in exons 13 and 19 with del 20 pb (3601-3620) in exon15. arabic 14 English 81
Refaat Tabagh, Ahmed Zaid(1-2018)
Publisher's website

Blocking of NF-kB/p38MAPK pathways mitigates oligodendrocyte pathology in a model of neonatal white matter injury

Reactive gliosis and inflammation are risk factors for white matter injury (WMI) development, which are correlated with the development of many neurodevelopmental deficits with no treatment. This study aimed to understand the mechanisms correlated with WMI, with a particular focus on the role of nuclear factor‑kappa B (NF‑kB) and p38 mitogen‑activated protein kinases (MAPKs) pathways. Seven‑day‑old Wistar rats were used to generate cerebellar tissue slices. Slices were cultured and randomly allocated to one of 3 groups and treated as follows: group‑I (control); group‑II (WMI), slices were subjected to 20 min of oxygen‑glucose deprivation (OGD); group‑III (WMI+ blockers), slices were subjected to OGD and treated with the blockers. Results showed that OGD insult triggered a marked increase in the apoptosis among WM elements, as confirmed by TUNEL assay. Immunocytochemical experiments revealed that there was a significant decrease in the percent of MBP+ OLs and NG2+ OPCs, and myelin integrity. There was also a significant increase in the percent of reactive microglia and astrocytes. BrdU immunostaining revealed there was an increase in the percent of proliferating microglia and astrocytes. Q‑RT‑PCR results showed OGD upregulated the expression levels of cytokines (TNF‑α, IL‑1, IL‑6, and IL‑1β) and inducible nitric oxide synthase (iNOS). On the other hand, treatment with BAY11 or SB203580 significantly enhanced the OL survival, restored myelin loss, and reduced microglia and astrocyte reactivity, and downregulated the iNOS and cytokine expression. Our findings demonstrate that blocking of NF‑KB/p38 MAPK pathways alleviated reactive gliosis, inflammation, and OL loss upon WMI. The findings may help to develop therapeutic interventions for WMI.
Mohamed A. Al-Griw, Michael G. Salter, Ian C. Wood(1-2022)
Publisher's website


The GC-box is an important transcriptional regulatory element present in the promoters of many mammalian genes, and is found in most, if not all, oxidative phosphorylation (OXPHOS) promoters. In the present study we examine the effects of three Sp1 family members (Sp2, Sp3, and Sp4) on the adenine nucleotide translocase 2, cytochrome c1, F1-ATPase β-subunit, and the mitochondria transcription factor (mtTFA) promoters in Drosophila SL2 cell line. Sp3, like Sp1, strongly activates transcription all four promoters. SP4 stimulates, moderately, but Sp2 had no effect. In addition, Sp3 can, like Sp1, inhibit transcription from the proximal promoter of the ANT2 gene through binding to the Cbox GC element. By contrast, Sp4 and Sp2 do not repress promoter activity. Furthermore, since Sp4 and Sp2 bind to the Cbox repression element on the ANT2 promoter, but do not repress transcription, inhibition of transcription … arabic 21 English 97
Ahmed Zaid(1-2012)
Publisher's website