RMIT University, Australia
Ali received the Bachelor of Clinical Laboratory Sciences, College of Applied Medical Sciences from King Saud University in Riyadh, KSA in 2005, and the Master of Laboratory Medicine from RMIT University in 2010, a master research in the Cytogenetic and Molecular Cytogenetic Laboratories of the Murdoch Children Research Institute in Melbourne.
He worked as medical technologist 1 in biochemistry lab in King Fahad Medical City 2006-2008 and 2011. His work involved the testing of quality control of the automated machines, analyzing and reporting blood samples for general biochemistry tests.
He is currently a PhD at RMIT University, and A lecturer in the Laboratory Medicine Department at Al-Baha University.
Ali currently research is study the evaluation of effectiveness and safety of Chinese medicine in the treatment of non-alcoholic fatty liver disease and liver-related disease. The common research topics include Molecular Biology, Metabolic Syndrome and Liver Diseases.
Non-alcoholic steatohepatitis (NASH) is an advanced stage of the metabolic syndrome in liver with serious consequences largely because of hepatic injury, inflammation and fibrosis. Matrine (MW: 248) is used as a prescribed hepatoprotective drug in humans and it has been shown by us to decrease hepatosteatosis and glucose intolerance in high fat-fed mice (Bri J Pharmacol 172:4303,2015). Here, we investigated whether matrine exerts therapeutic efficacy for NASH by attenuating hepatic injury, inflammation and fibrosis. The study was performed in methionine choline-deficient (MCD) diet-fed mice for 6 weeks with or without the treatment with matrine (100 mg/kg/d). Compared with untreated MCD-fed mice, matrine markedly reduced hepatic injury (indicated by ALT level, p<0.05), inflammation (indicated by TNFα, CD68 and inflammasome NLRP3, all p<0.05). Along with these effects, matrine inhibited MCD-induced increases in fibrogenesis (as indicated by the expression levels of TGFβ, Smad3 and type I collagen (all p<0.05). Further examination revealed that matrine resecured MCD-suppressed heat shock protein 72 (HSP72, a protective chaperon protein against cell toxicity) and inhibited MCD-activated mTOR (a key master regulator triggering pathogenic pathways leading to NASH). Our findings indicate that matrine attenuated MCD-induced NASH by a new mechanism involving the upregulation of HSP72 and inhibition of mTOR. This hepatoprotective drug may be repurposed for the treatment of NASH.