Displaying all 2 publications

Abstract:
Sort:
  1. Fulltext Drug Development
    Majeed ABA, Ramasamy K, Tan MP, LIm SM, Hui KM, Tan AH, et al.
    Alzheimers Dement, 2024 Dec;20 Suppl 6(Suppl 6):e093563.
    PMID: 39782435 DOI: 10.1002/alz.093563
    BACKGROUND: Gut microbiota modulation of the brain function may present an opportunity to devise preventive or treatment strategies to manage impairments such as cognitive frailty (CF). This study aims to uncover the relationship between CF, gut microbiota, intestinal permeability and proteome.

    METHOD: A total of 137 fecal samples of the elderly were collected, and subjected to DNA analysis, and enzyme-linked immunosorbent assays (ELISA). Plasma samples were subjected to mass spectrometry proteomic analysis. The parameters of the subjects measured include functional reach test (FRT), handgrip strength (HGS), Visual Cognitive Assessment Test (VCAT), Montreal Cognitive Assessment (MoCA), timed up and go (TUG) and UCLA three-item loneliness scale (UCLA-3).

    RESULT: At the genus level, Alistipes which are potential drivers of dysbiosis, are significantly increased in CF subjects. Proteobacteria are also negatively linked to FRT, HGS, VCAT, and MoCA, but positively correlated to TUG and UCLA-3. Lactoferrin was upregulated in pre-frail subjects. The plasma apolipoprotein AI (Apo-AI) was upregulated 5 times in the CF subjects.

    CONCLUSION: These findings provide evidence for dietary intervention to alter gut microbiota that may modulate cognitive status.

  2. Fulltext A novel benzimidazole derivative, MBIC inhibits tumor growth and promotes apoptosis via activation of ROS-dependent JNK signaling pathway in hepatocellular carcinoma
    Dai X, Wang L, Deivasigamni A, Looi CY, Karthikeyan C, Trivedi P, et al.
    Oncotarget, 2017 Feb 21;8(8):12831-12842.
    PMID: 28086233 DOI: 10.18632/oncotarget.14606
    A prior screening programme carried out using MTT assay by our group identified a series of novel benzimidazole derivatives, among which Methyl 2-(5-fluoro-2-hydroxyphenyl)-1H- benzo[d]imidazole-5-carboxylate (MBIC) showed highest anticancer efficacy compared to that of chemotherapeutic agent, cisplatin. In the present study, we found that MBIC inhibited cell viability in different hepatocellular carcinoma (HCC) cell lines without exerting significant cytotoxic effects on normal liver cells. Annexin V-FITC/PI flow cytometry analysis and Western blotting results indicated that MBIC can induce apoptosis in HCC cells, which was found to be mediated through mitochondria associated proteins ultimately leading to the activation of caspase-3. The exposure to MBIC also resulted in remarkable impairment of HCC cell migration and invasion. In addition, treatment with MBIC led to a rapid generation of reactive oxygen species (ROS) and substantial activation of c-Jun-N-terminal kinase (JNK). The depletion of ROS by N-Acetyl cysteine (NAC) partially blocked MBIC-induced apoptosis and JNK activation in HCC cells. Finally, MBIC significantly inhibited tumor growth at a dose of 25 mg/kg in an orthotopic HCC mouse model. Taken together, these results demonstrate that MBIC may inhibit cell proliferation via ROS-mediated activation of the JNK signaling cascade in HCC cells.
Related Terms
    Try searching for something
Filters
Contact Us

Please provide feedback to Administrator (afdal@afpm.org.my)

External Links