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  1. Effects of 17β estradiol on blood pressure elevation in ovariectomized rats with collagen-induced arthritis via modulation of oxidative stress, inflammation, fibrosis, and apoptosis in the aorta involving TLR4/NOX4/NF-kβ and TGFβ1/fibronectin/α-SMA pathways
    Govindasamy N, Barman M, Salleh N, Giribabu N, Shahzad H
    Naunyn Schmiedebergs Arch Pharmacol, 2024 Dec 19.
    PMID: 39702602 DOI: 10.1007/s00210-024-03700-9
    Rheumatoid arthritis (RA) can cause blood pressure (BP) elevation in estrogen-deficient, post-menopausal women; however, the underlying mechanisms are not well understood. In this study, the aortic involvement and its underlying mechanisms that contribute to the BP elevation in estrogen-deficient, RA condition were identified. Ovariectomy was performed to create a state of estrogen deficiency and RA was then induced in ovariectomized rats by using incomplete Freund's adjuvant and immune-mediated collagen type-II. Ovariectomized, RA-induced rats (Ovx + RA) were given either 17β-estradiol, baricitinib, or losartan. Direct blood pressure (BP) monitoring was made via cannulation of the carotid artery. Rats were then sacrificed and the aorta was harvested followed by H&E and Picrosirius staining to evaluate histological changes and collagen deposition. Oxidative stress, inflammation, apoptosis, growth, and fibrosis levels in the aorta were assessed by using molecular biological techniques. Mean arterial pressure (MAP) was significantly elevated in Ovx + RA rats when compared to sham and Ovx rats (p 
  2. Fulltext Melatonin Induced Schwann Cell Proliferation and Dedifferentiation Through NF-ĸB, FAK-Dependent but Src-Independent Pathways
    Govindasamy N, Chung Chok K, Ying Ng P, Yian Koh R, Moi Chye S
    Rep Biochem Mol Biol, 2022 Apr;11(1):63-73.
    PMID: 35765532 DOI: 10.52547/rbmb.11.1.63
    BACKGROUND: Peripheral nerve injury (PNI) is a common condition that compromises motor and sensory functions. Peripheral nerves are known to have regenerative capability and the pineal hormone, melatonin, is known to aid nerve regeneration. However, the role of Schwann cells and the pathways involved remain unclear. Thus, the aim of this study is to identify the effects of melatonin on Schwann cell proliferation, dedifferentiation, and the involvement of nuclear factor kappa light chain enhancer of activated B cells (NF-ĸB), focal adhesion kinase (FAK) and proto-oncogene tyrosine-protein kinase, Src pathways in this process.

    METHODS: Schwann cells was treated with melatonin and its proliferation and dedifferentiation were identified using MTT assay and immunofluorescence staining for SRY (sex determining region Y)-box 2 (SOX2). Next, the protein expressions of NF-ĸB, FAK and Src pathways were identified by Western blot.

    RESULTS: MTT results confirmed increased proliferation of Schwann cells with melatonin treatment, and it was highest at 10 μM melatonin. Immunofluorescent staining revealed an increase in the green fluorescence staining for SOX2 in melatonin-treated cells, showing enhanced dedifferentiation. Western blot assay revealed melatonin increased phospho-NF-ĸB (PNF-ĸB), IKK-α, FAK (D2R2E), phospho-FAK (Tyr 576/577 and Tyr 397) protein expressions as compared with control. However, Src (32G6), Lyn (C13F9), Fyn, Csk (C74C1) protein expressions were not increased as compared with control.

    CONCLUSION: Melatonin promotes Schwann cell proliferation and dedifferentiation via NF-ĸB, FAK-dependent but Src-independent pathways.

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