1Salim Nasser al-ryashi and 2Ali-G. Al-Kaf
1Department ofAnatomy and Histology, Faculty of Medicine, Sana'a University
2Department of Medicinal Chemistry, Faculty of Pharmacy
Introduction:
Shilajit is a herbo-mineral, marine animal origin- dead/fossil invertebrates, semi-hard brownish black resin formed through long-term humification of several plant types, mainly bryophytes such as Euphorbia and Trifolium (clover) plants and lichen, present in the vicinity of shilajit-exuding rocks. This plant type of shilajit called Mumie-asil to being distinguished from other types (petroleum mumie and mumie- kiem). It has common names; vegetable asphalt, mineral pitch, mountain sweat, mountain oil, rock juice. The name ‘‘mumie, hajar-musa or mumia’’ was devised by the Arabs and in ancient Egypt, this wonderful resin was used for embalming mummies (1,2,3,4).
It is found in specific mountain regions of the world at altitudes between 0.6 and 5 km on the walls of caves, embedded in rocks or as rock exudates and can exceed 500 kg in weight; inKashmir, Afghanistan, Nepal, Bhutan, Pakistan, China, Tibet, Yemen, Asian parts of Russia and neighboring areas (5,4). Its samples from different regions of the world have similar physical properties and
qualitative chemical composition but they differ in the ratio of individual components (6). Shilajit humus consists of organic matter (60-80%), mineral matter (20-40%) and 5% trace elements. The main chemical components of shilajit are humic acid, fulvic acid, benzoic acid, benzoates andhigh concentration of vitamin A, B, C esters (7,1). Modern chemical analyses identified six new compounds named as shilajityl acetate, shilajitol, shilacatechol, shilaxanthone, shilanthranil and naphsilajitone along with pyrocatechol and their stereostructures (2). It traditionally used for obstinate diseases including; tuberculosis, cervical lymphadenitis, diabetes mellitus-type I, digestive disorders, cough, obesity, hemorrhoids, Jaundice, poison begotten distempers and internal tumors (8).
Mucosal injury may occur when noxious factors “overwhelm” an intact mucosal defense or when the mucosal defense is somehow impaired (9). Ethanol induced gastric damage has been soon to be associated with depletion of gastric mucus breaking of the mucosal barrier, back diffusion of acid, increased gastric mucosal
