ArticleElectronic physician2017
Caspase 3 role and immunohistochemical expression in assessment of apoptosis as a feature of H1N1 vaccine-caused Drug-Induced Liver Injury (DILI).
Article in Electronic physician, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 16 citations in OpenAlex.
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- TLR-4/Notch1/NF-κB pathway modulation by dapagliflozin: a novel mechanism for neuroprotection in hepatic encephalopathy.Metabolic brain disease · 2025Article
- Fatty acids homeostasis during fasting predicts protection from chemotherapy toxicity.Nature communications · 2022Article
- Protective Effects of Magnesium Glycyrrhizinate on Methotrexate-Induced Hepatotoxicity and Intestinal Toxicity May Be by Reducing COX-2.Frontiers in pharmacology · 2019Article
- Sulforaphane protects against LPS-induced liver injury in mice by antagonizing oxidative stress and apoptosis through AMPK activation.International journal of health sciencesArticle
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDrug-Induced Liver Injury (DILI) changes, occur post exposure to natural or chemical compounds including apoptosis.
aimTo assess the H1N1 vaccine-caused DILI by histochemical and immunohistochemical methods.
methodsThis 2014's experimental study was conducted on 70 albino rats. They were given Arepanrix
resultsHistopathological changes ranging from subtle up to necrosis were noticed, mainly in mix groups. Metabolic protein and glycogen changes were the maximum in mix5 group (p<0.01). Collagen deposition in sinusoids was higher in mix groups, and maximally in vac5 and mix5. Apoptotic hepatocytes expressing diffuse strong nuclear and cytoplasmic caspase 3 were the highest in mix5.
conclusionH1N1 vaccine can cause DILI by either direct toxic or idiosyncratic metabolic type reactions rather than immunologic hypersensitivity type. It ranges from subtle changes up to necrosis. Caspase 3 is pivotal in liver damage etiology, apoptosis induction and processing. Follow up for at least 2 months after the 2
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