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  1. Analyzed Page
  2. Matching Content Categories
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We began analyzing https://link.springer.com/article/10.1007/s00210-022-02264-w, but it redirected us to https://link.springer.com/article/10.1007/s00210-022-02264-w. The analysis below is for the second page.

Title[redir]:
Association of resveratrol with the suppression of TNF-α/NF-kB/iNOS/HIF-1α axis-mediated fibrosis and systemic hypertension in thioacetamide-induced liver injury | Naunyn-Schmiedeberg's Archives of Pharmacology
Description:
Chronic liver injury can lead to hepatic failure and the only available method of treatment would be liver transplantation. The link between inflammation (TNF-α), nuclear factor-kappa B (NF-kB), nitrosative stress (iNOS) and hypoxia-inducible factor-1α (HIF-1α) in thioacetamide (TAA) induced liver fibrosis, and hypertension with and without the incorporation of the anti-inflammatory and antioxidant resveratrol (RES) has not been investigated before. Consequently, we injected rats with either 200 mg/kg TAA for 8 weeks starting at week 2 (model group) or pretreated them before TAA injections with RES (20 mg/kg) for 2 weeks and continued them on RES and TAA until being culled at week 10 (protective group). In the model group, we documented the induction of hepatic fibrosis and upregulation of tumor necrosis factor-α (TNF-α), NF-kB, inducible nitric oxide synthase (iNOS), HIF-1α and the profibrotic biomarkers alpha-smooth muscle actin (α-SMA) and matrix metalloproteinase-9 (MMP-9) that was significantly (p ≤ 0.0014) ameliorated by RES. RES also significantly (p ≤ 0.0232) reduced triglycerides (TG), cholesterol (CHOL), very low-density lipoprotein (vLDL-C), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure, and heart rate (HR) induction by TAA. Also, a significant (p < 0.0001) positive correlation between TNF-α/NF-kB/iNOS/HIF-1α axis-mediated fibrosis and hypertension and liver injury biomarkers was observed. These findings suggest that in the hepatotoxic compound, TAA is associated with TNF-α/NF-kB/iNOS/HIF-1α-mediated fibrosis and hypertension, whilst being inhibited by RES.

Matching Content Categories {📚}

  • Health & Fitness
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  • Science

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

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Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🏙️ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 98,426,998 visitors per month in the current month.

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The income method remains a mystery to us.

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Keywords {🔍}

article, google, scholar, cas, liver, fibrosis, resveratrol, hypertension, cells, hepatic, data, alani, lin, injury, university, res, rats, wang, department, medicine, research, taa, access, author, cell, hepatol, cairo, privacy, cookies, content, information, publish, thioacetamideinduced, kamar, mohamed, chronic, model, expression, stellate, inhibits, yang, search, tnfαnfkbinoshifα, manuscript, haidara, abd, ellatif, amal, dawood, inflammation,

Topics {✒️}

tnf-α/nf-kb/inos/hif-1α axis-mediated fibrosis tnf-α/nf-kb/inos/hif-1α-mediated fibrosis nf-κb/tnf-α pathway cyclophosphamide-induced multi-organ toxicity hypoxia-inducible factor-1α tumor necrosis factor-α thioacetamide-induced liver fibrosis thioacetamide-induced liver injury month download article/chapter common nfκb-inos pathway acetaminophen-induced liver fibrosis thioacetaide-induced liver injury dr mariam al-ani hypoxia-induced pulmonary hypertension cholesterol-induced liver fibrosis thioacetamide-induced liver cirrhosis kasr al-aini faculty tnf-alpha release hif-1α inhibiting hif-1alpha nf-kb induced liver fibrosis references  al-ani cgmp-dependent protein kinase hif-{alpha} isoforms tnf-α tnf-alpha levels 5′-activated protein kinase resveratrol ameliorates fibrosis liver injury biomarkers chronic liver disease human endothelial cells hepatic stellate cells article naunyn-schmiedeberg' collagen production induced progressive liver fibrosis liver–linking injury nf-kappab activation hypoxia-inducible factors mtor-dependent pathway experimental liver research nuclear factor-kappa full article pdf mohamed abd ellatif privacy choices/manage cookies resveratrol inhibits proliferation inos expression aβ-induced neurotoxicity nf-κb selectively induces apoptosis

Schema {🗺️}

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         headline:Association of resveratrol with the suppression of TNF-α/NF-kB/iNOS/HIF-1α axis-mediated fibrosis and systemic hypertension in thioacetamide-induced liver injury
         description:Chronic liver injury can lead to hepatic failure and the only available method of treatment would be liver transplantation. The link between inflammation (TNF-α), nuclear factor-kappa B (NF-kB), nitrosative stress (iNOS) and hypoxia-inducible factor-1α (HIF-1α) in thioacetamide (TAA) induced liver fibrosis, and hypertension with and without the incorporation of the anti-inflammatory and antioxidant resveratrol (RES) has not been investigated before. Consequently, we injected rats with either 200 mg/kg TAA for 8 weeks starting at week 2 (model group) or pretreated them before TAA injections with RES (20 mg/kg) for 2 weeks and continued them on RES and TAA until being culled at week 10 (protective group). In the model group, we documented the induction of hepatic fibrosis and upregulation of tumor necrosis factor-α (TNF-α), NF-kB, inducible nitric oxide synthase (iNOS), HIF-1α and the profibrotic biomarkers alpha-smooth muscle actin (α-SMA) and matrix metalloproteinase-9 (MMP-9) that was significantly (p ≤ 0.0014) ameliorated by RES. RES also significantly (p ≤ 0.0232) reduced triglycerides (TG), cholesterol (CHOL), very low-density lipoprotein (vLDL-C), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure, and heart rate (HR) induction by TAA. Also, a significant (p < 0.0001) positive correlation between TNF-α/NF-kB/iNOS/HIF-1α axis-mediated fibrosis and hypertension and liver injury biomarkers was observed. These findings suggest that in the hepatotoxic compound, TAA is associated with TNF-α/NF-kB/iNOS/HIF-1α-mediated fibrosis and hypertension, whilst being inhibited by RES.
         datePublished:2022-06-22T00:00:00Z
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      headline:Association of resveratrol with the suppression of TNF-α/NF-kB/iNOS/HIF-1α axis-mediated fibrosis and systemic hypertension in thioacetamide-induced liver injury
      description:Chronic liver injury can lead to hepatic failure and the only available method of treatment would be liver transplantation. The link between inflammation (TNF-α), nuclear factor-kappa B (NF-kB), nitrosative stress (iNOS) and hypoxia-inducible factor-1α (HIF-1α) in thioacetamide (TAA) induced liver fibrosis, and hypertension with and without the incorporation of the anti-inflammatory and antioxidant resveratrol (RES) has not been investigated before. Consequently, we injected rats with either 200 mg/kg TAA for 8 weeks starting at week 2 (model group) or pretreated them before TAA injections with RES (20 mg/kg) for 2 weeks and continued them on RES and TAA until being culled at week 10 (protective group). In the model group, we documented the induction of hepatic fibrosis and upregulation of tumor necrosis factor-α (TNF-α), NF-kB, inducible nitric oxide synthase (iNOS), HIF-1α and the profibrotic biomarkers alpha-smooth muscle actin (α-SMA) and matrix metalloproteinase-9 (MMP-9) that was significantly (p ≤ 0.0014) ameliorated by RES. RES also significantly (p ≤ 0.0232) reduced triglycerides (TG), cholesterol (CHOL), very low-density lipoprotein (vLDL-C), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure, and heart rate (HR) induction by TAA. Also, a significant (p < 0.0001) positive correlation between TNF-α/NF-kB/iNOS/HIF-1α axis-mediated fibrosis and hypertension and liver injury biomarkers was observed. These findings suggest that in the hepatotoxic compound, TAA is associated with TNF-α/NF-kB/iNOS/HIF-1α-mediated fibrosis and hypertension, whilst being inhibited by RES.
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         Liver fibrosis
         Hypertension
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         Resveratrol
         TNF-α/NF-kB/iNOS/HIF-1α axis
         Pharmacology/Toxicology
         Neurosciences
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External Links {🔗}(178)

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