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Platelet markers [soluble p selectin (sP-selectin) and soluble CD40 ligand (sCD40L)] are associated with platelet activation and cardiovascular risk. Both policosanol and 10-dehydrogingerdione are natural products with proven CETP inhibitory and antiatherogenic effects. Present work aimed mainly to investigate the levels of platelet activation biomarkers in the serum of dyslipidemic rabbits and the potential of these phytochemicals either alone or in a combination form to protect against atherogenicity. Additionally, this work clarified their effect on PCSK9, a key player in atherosclerosis progression. Daily administration of policosanol and/or 10-dehydrogingerdione at a dose level 10 mg/kg bw resulted in a CETP inhibitory activity, increasing HDL-C level. This protective effect was associated with improvement in lipid profile components and a reduction in PCSK9 level. Interestingly, this combination strengthened the CETP inhibitory activity of these phytochemicals, leading to a greater increase in serum HDL-C level than monotherapy. However, this combination did not enhance the reduction in PCSK9 level. Both drugs also decreased platelet activation and inflammation markers such as sCD40L, sP-selectin, and interferon-gamma (IFN-gamma), and their combination showed a synergistic effect. Therefore, such phytochemicals may be regarded as promising agents in the protection against atherothrombosis risk.


Atherogenesis CETP Dyslipidemia PCSK9 Policosano

Gingival crevicular fluid levels of human beta-defensin-1 in type 2 diabetes mellitus and periodontitis

Posted by D Yilmaz, F Caglayan, E Buber, et al. on 2018-05-24 20:24:40



Human beta-defensin (hBD)-1 is an important gatekeeper of the gingiva against constant bacterial challenge, and glucose levels are involved in its optimal expression. The aims of the study were to investigate hBD-1 levels in gingival crevicular fluid (GCF) and to compare these levels between type 2 diabetics with or without periodontitis and healthy individuals.

Materials and methods

Altogether, 81 subjects were included in the study: 21 subjects with type 2 diabetes mellitus (T2DM) suffering from generalized periodontitis (T2DM + GP), 18 systemically healthy generalized periodontitis patients (GP), 18 periodontally healthy T2DM subjects (T2DM+H), and 24 systemically and periodontally healthy subjects (control). Plaque index (PI), gingival index (GI), probing pocket depth (PPD), and clinical attachment level (CAL) were recorded, and GCF samples were collected. hBD-1 levels in GCF were measured using ELISA.


hBD-1 levels were significantly reduced in the T2DM + GP and GP groups. Although PI and GI scores were similar in both periodontally healthy groups, hBD-1 levels were lower in the T2DM + H group. In the whole population, hBD-1 levels correlated negatively with all periodontal parameters.


Both diabetes and periodontitis affect hBD-1 levels in GCF.

Clinical relevance

The altered levels of hBD-1 in GCF of diabetics might be associated with the susceptibility of diabetics to periodontitis.


Antimicrobial peptides Diabetes mellitus Periodontitis Gingival crevicular fluid


Liver fibrosis is a major health issue leading to high morbidity and mortality. The potential anti-fibrotic activity and the effect of mesalazine on osteopontin (OPN), an extra cellular matrix (ECM) component were evaluated in TAA-induced liver fibrosis in rats. For this purpose, forty-two adult male Wistar rats were divided into six groups. All animals, except the normal control, were intraperitoneally injected with TAA (200?mg/kg) twice per week for 6 weeks. In the hepato-protective study, animals were administered mesalazine (50 and 100?mg/kg, orally) for 4 weeks before induction of liver fibrosis then concomitantly with TAA injection. In the hepato-therapeutic study, animals were administered mesalazine for 6 weeks after TAA discontinuation with the same doses. In both studies, mesalazine administration improved liver biomarkers through decreasing serum levels of AST, ALT and total bilirubin when compared to fibrotic group with significant increase in total protein and albumin levels. Mesalazine significantly decreased hepatic MDA level and counteracted the depletion of hepatic GSH content and SOD activity. Additionally, it limits the elevation of OPN and TGF-beta1 concentrations and suppressed TNF-alpha as well as alpha-SMA levels in hepatic tissue homogenate. Histopathologically, mesalazine as a treatment showed a good restoration of the hepatic parenchymal cells with an obvious decreased intensity and retraction of fibrous proliferation, while as a prophylaxis it didnot achieve enough protection against the harmful effect of TAA, although it decreased the intensity of portal to portal fibrosis and pseudolobulation. Furthermore, mesalazine could suppress the expression of both alpha-SMA and caspase-3 in immunohistochemical sections. In conclusion, mesalazine could have a potential new indication as anti-fibrotic agent through limiting the oxidative damage and altering TNF-alpha pathway as an anti-inflammatory drug with down-regulating TGF-beta1, OPN, alpha-SMA and caspase-3 signaling pathways.

Topiramate mitigates 3-nitropropionic acid-induced striatal neurotoxicity via modulation of AMPA receptors

Posted by H N. Shalaby, D M. EI-Tanbouly, H F. Zaki. on 2018-05-24 18:53:06


Prevalence of glutamate receptor subunit 2 (GluR2)-lacking alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors is a hallmark of excitotoxicity-related neurodegenerative diseases. Topiramate (TPM) is a structurally novel anticonvulsant with a well-known modulatory effects on AMPA/kainate subtypes of glutamate receptors. The present study aimed at investigating the neuroprotective potential of TPM on 3-nitropropionic acid (3-NP)-induced striatal neurodegeneration and Huntington disease-like symptoms. Rats were injected with 3-NP (10?mg/kg/i.p.) for 14 days. TPM (50?mg/kg/p.o.) was given once a day, 1?h before 3-NP. TPM amended 3-NP induced changes in neurobehavioral performance, striatal neurotransmitters levels and histopathological injury. 3-NP control rats showed a significant ablation in the mRNA expression of Ca2+-impermeable Glu2R subunit along with an elevation in its regulatory protein (protein interacting with C kinase-1) PICK1, an effect that was largely reversed by TPM. TPM in addition, enhanced the phosphorylation of the protein kinase B/glycogen synthase kinase-3beta/cAMP response element binding protein (Akt/GSK-3beta/CREB) cue. Moreover, improvement in oxidative status, suppression of caspase-3 activity and restoration of striatal BDNF were noticed following treatment with TPM. The current study revealed that TPM boosted the neuroprotective (Akt/GSK-3beta/CREB) pathway by its negative modulatory effect on AMPA glutamate receptors as well as its direct antioxidant property.


Excessive nuclear factor-kB (NF-kB) activation mediated by tumor necrosis factor alpha (TNF alpha) plays a critical role in inflammation. Here we demonstrate that angiopoietin-like 8 (ANGPTL8) functions as a negative feedback regulator in TNF alpha-triggered NF-kB activation intracellularly. Inflammatory stimuli induce ANGPTL8 expression, and knockdown or knockout of ANGPTL8 potentiates TNF alpha-induced NF-kB activation in vitro. Mechanistically, upon TNF alpha stimulation, ANGPTL8 facilitates the interaction of IKK gamma with p62 via forming a complex, thus promoting the selective autophagic degradation of IKK gamma. Furthermore, the N-terminal domain mediated self-oligomerization of ANGPTL8 is essential for IKK gamma degradation and NF-kB activation. In vivo, circulating ANGPTL8 level is high in patients diagnosed with infectious diseases, and the ANGPTL8/p62-IKK gamma axis is responsive to inflammatory stimuli in the liver of LPS-injected mice. Altogether, our study suggests the ANGPTL8/p62-IKK gamma axis as a negative feedback loop that regulates NF-kB activation, and extends the role of selective autophagy in fine-tuned inflammatory responses.

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