Saha Jamaluddin

Baylor College of Medicine, Houston, Texas, United States

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Publications (2)4.89 Total impact

  • Saha Jamaluddin · Zhengdong Liang · Jian-Ming Lü · Qizhi Yao · Changyi Chen
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    ABSTRACT: Cardiovascular disease remains the number one killer in the United States and many other countries. Each year, there are enormous research efforts on its pathogenesis, prevention and treatment led by scientists worldwide. One of the most significant research areas is the impact and mechanisms of existing or new cardiovascular risk factors on the vascular system. The current review provides the most updated research advances in the area of the regulation of the endothelial nitric oxide synthase-nitric oxide (eNOS-NO) system by several cardiovascular risk factors. There are many exciting discoveries made from the studies of several major cardiovascular risk factors such as hypertension, cigarette smoking, dyslipidemia and diabetes mellitus as well as emerging risk factors such as HIV infection, antiretroviral therapy, genomic variability, and cytokines. In general, cardiovascular risk factors could impair the eNOS-NO system with a variety of molecular mechanisms including decrease in NO bioavailability by excess reactive oxygen species, inhibition of eNOS expression and activity, and deficiency of eNOS cofactors. Special attention is paid to the impact of several new or emerging risk factors on cardiovascular disease and the eNOS-NO system. These mechanistic studies are clinically significant because they may lead towards new and effective strategies for the prevention and treatment of cardiovascular disease.
    No preview · Article · Oct 2013 · Current pharmaceutical design
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    ABSTRACT: Several HIV protease mutations, which are resistant to clinical HIV protease inhibitors (PIs), have been identified. There is a great need for second-generation PIs with different chemical structures and/or with an alternative mode of inhibition. Ginkgolic acid is a natural herbal substance and a major component of the lipid fraction in the nutshells of the Ginkgo biloba tree. The objective of this study was to determine whether ginkgolic acid could inhibit HIV protease activity in a cell free system and HIV infection in human cells. Purified ginkgolic acid and recombinant HIV-1 HXB2 KIIA protease were used for the HIV protease activity assay. Human peripheral blood mononuclear cells (PBMCs) were used for HIV infection (HIV-1SF162 virus), determined by a p24gag ELISA. Cytotoxicity was also determined. Ginkgolic acid (31.2 µg/ml) inhibited HIV protease activity by 60%, compared with the negative control, and the effect was concentration-dependent. In addition, ginkgolic acid treatment (50 and 100 µg/ml) effectively inhibited the HIV infection at day 7 in a concentration-dependent manner. Ginkgolic acid at a concentration of up to 150 µg/ml demonstrated very limited cytotoxicity. Ginkgolic acid effectively inhibits HIV protease activity in a cell free system and HIV infection in PBMCs without significant cytotoxicity. Ginkgolic acid may inhibit HIV protease through different mechanisms than current FDA-approved HIV PI drugs. These properties of ginkgolic acid make it a promising therapy for HIV infection, especially as the clinical problem of viral resistance to HIV PIs continues to grow.
    Preview · Article · Aug 2012 · Medical science monitor: international medical journal of experimental and clinical research