Publications by authors named "Somayeh M Baram"

Article Synopsis
  • Acetyl-11-keto-beta-boswellic acid (AKBA) is an anti-inflammatory compound studied for its effectiveness in preventing and treating non-alcoholic fatty liver disease (NAFLD) in male Wistar rats.
  • The study included groups treated with AKBA either during a high fructose diet for 6 weeks or after switching to a normal diet for 2 weeks, analyzing various liver-related parameters and inflammatory markers.
  • Results indicated that AKBA improved liver health indicators and inflammation, supported lipid metabolism, and helped maintain crucial proteins that regulate cellular energy, suggesting it could be a potential treatment for NAFLD.
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Background: Alzheimer's disease (AD) is the main cause of the neurodegenerative disorder, which is not detected unless the cognitive deficits are manifested. An early prediagnostic specific biomarker preferably detectable in plasma and hence non-invasive is highly sought-after. Various hypotheses refer to AD, with amyloid-beta (Aβ) being the most studied hypothesis and inflammation being the most recent theory wherein pro-and anti-inflammatory cytokines are the main culprits.

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Experimental autoimmune encephalomyelitis (EAE) as an experimental model of multiple sclerosis (MS) is characterized by demyelination, infiltration of inflammatory cells into the nervous system and dysregulation of serum inflammatory cytokines. We investigated the correlation of serum cytokines and other inflammatory markers with the EAE pathogenesis. After EAE induction, the levels of different serum cytokine/inflammatory mediators were measured.

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Ischaemic stroke represents one of the main causes of disability. According to the broad investigations, it is widely assumed that the contribution of inflammatory mediators is strongly involved in its pathogenesis. Hence, it seems that stroke treatment needs more efficient and inflammatory-targeted compounds to modulate inflammatory-related pathways.

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Doxorubicin is an effective chemotherapeutic drug against a considerable number of malignancies. However, its toxic effects on myocardium are confirmed as major limit of utilization. PPAR-α is highly expressed in the heart, and its activation leads to an increased cardiac fatty acid oxidation and cardiomyocyte necrosis.

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