Stroke remains a debilitating cerebrovascular condition associated with oxidative stress, while COVID-19 has emerged as a global health crisis with multifaceted systemic implications. This study investigates the hypothesis that patients experiencing acute ischemic stroke alongside COVID-19 exhibit elevated oxidative stress markers and altered antioxidant defense mechanisms compared to those with acute ischemic stroke. We conducted a single-center prospective cross-sectional study to investigate oxidative stress balance through oxidative damage markers: TBARS (thiobarbituric acid reactive substances level) and PCARB (protein carbonyls); antioxidant defense mechanisms: TAC (total antioxidant capacity), GPx (glutathione peroxidase), GSH (reduced glutathione), CAT (catalase), and SOD (superoxide dismutase); as well as inflammatory response markers: NLR (neutrophil-to-lymphocyte ratio), CRP (C-reactive protein), and ESR (erythrocyte sedimentation rate). Statistical analyses and correlation models were employed to elucidate potential associations and predictive factors. Our results revealed increased oxidative stress, predominantly indicated by elevated levels of TBARS in individuals experiencing ischemic stroke alongside a concurrent COVID-19 infection (p < 0.0001). The Stroke-COVID group displayed notably elevated levels of GSH (p = 0.0139 *), GPx (p < 0.0001 ****), SOD (p = 0.0363 *), and CAT (p = 0.0237 *) activities. Multivariate analysis found a significant association for TBARS (p < 0.0001 ****), PCARB (p = 0.0259 *), and GPx activity (p < 0.0001 ****), together with NLR (p = 0.0220 *) and CRP (p = 0.0008 ***). Notably, the interplay between stroke and COVID-19 infection appears to amplify oxidative damage, potentially contributing to exacerbated neurological deficits and poorer outcomes. This study highlights the intricate relationship between oxidative stress, inflammation, and concurrent health conditions. Understanding these interactions may open avenues for novel therapeutic strategies aimed at ameliorating oxidative damage in patients with acute ischemic stroke and COVID-19, ultimately improving their prognosis and quality of life.

Inflammation and the injuries produced by free radicals are interconnected and influence each other. The underlying mechanisms of inflammation are partially attributed to the release of free radicals by immune cells, prooxidants that can also cause protein alteration. This study was performed in order to assess the potential anti-inflammatory effect of two bee venom samples harvested from Apis mellifera. Free radical scavenging capacity was investigated using DPPH and ABTS.+ tests and protective effect on proteins through the inhibitory activity on thermal denaturation of albumin.

Polyphenols are key dietary bioactive compounds, reducing oxidative stress and neurodegeneration. This study investigated the in vitro antioxidant and neuroprotective potential of some edible fruits (apricots, plums, figs) and vegetable (parsley) extracts related to their phytochemical profile. Plum extract exhibited the strongest antioxidant capacity (ABTS IC₅₀ 1.733 ± 0.079 mg/g; DPPH IC₅₀ 1.593 ± 0.069 mg/g; FRAP 23.161 ± 1.094 mM Fe²⁺), linked to its high chlorogenic and caffeic acids content. Parsley displayed the most potent AChE inhibition (IC₅₀ 0.825 ± 0.026 mg/g), associated with an elevated flavonoids level (TFC 12.874 ± 0.534 mg QE/g) and the presence of ferulic and vanillic acids. Apricot was characterized by notable gallic, syringic, and chlorogenic acids, supporting moderate neuroprotective potential. Figs showed weaker radical scavenging ability but provided a balanced profile of protocatechuic, caffeic, and syringic acids. Correlation analysis revealed specific compound–activity associations, including syringic and vanillic acids with DPPH scavenging capacity, p-coumaric acid with TPC, and gallic/ferulic acids with AChE inhibition. Effect-directed HPTLC confirmed chlorogenic acid as a major contributor to the antioxidant capacity. To our knowledge, this is the first study to comparatively integrate spectrophotometric antioxidant assays, UHPLC-based quantitative phenolic profiling, effect-directed HPTLC bioautography, and AChE inhibition analysis across three edible fruits and one vegetable frequently co-consumed in Mediterranean-type diets, enabling a cross-species compound–activity correlation framework. These species exhibit distinct but complementary phytochemical and biofunctional profiles. Their combined use may support the formulation of functional foods with synergistic antioxidant and neuroprotective benefits.

Background/Objectives: Platelet-rich plasma (PRP)–based regimens are widely used in non-scarring alopecia, yet objective response is variable and clinic-ready predictors are lacking. We evaluated short-term trichoscopic outcomes in routine practice and tested whether baseline complete blood count–derived inflammatory status, quantified by the neutrophil-to-lymphocyte ratio (NLR), can stratify response under PRP-based therapy. Methods: We performed an ambispective observational cohort study (October 2024–October 2025) in an outpatient dermatology practice. The final analytic cohort included 129 patients allocated to four treatment groups: PRP alone (n = 54), PRP combined with microneedling-assisted Purasomes Hair & Scalp Complex (HCS50+, Dermoaroma; exosome-containing) (n = 33), PRP combined with microneedling-assisted Mesoaroma Hair Cocktail (scalp formulation; nutrient complex) (n = 24), and a nutrient complex alone (n = 18). Trichoscopy (FotoFinder ATBM; FotoFinder Systems GmbH, Bad Birnbach, Germany) was obtained at baseline (T1) and first follow-up (T2). Density response was defined as a ≥10% increase in total hair density and hair-cycle response as an anagen fraction increase ≥5 percentage points. Predictive analyses were prespecified and restricted to PRP-containing regimens, using logistic regression and a multilayer perceptron with repeated cross-validation for internal validation. Results: Across the full cohort (n = 129), total hair density and hair-cycle parameters improved from T1 to T2. In the PRP-containing subgroup (n = 111), baseline NLR strongly discriminated density responders (AUC 0.85, bootstrap 95% CI 0.77–0.91). In multivariable models, NLR remained independently associated with density response (OR 0.31 per 1-unit increase, 95% CI 0.20–0.48). Conclusions: In this cohort, baseline NLR was associated with discrimination of early trichoscopic response in PRP-based treatment of non-scarring alopecia. Using the Youden-derived cut-off (NLR = 2.202), patients with NLR > 2.202 had a higher risk of density non-response (72.1% vs. 4.7%), corresponding to a 15.49-fold increased failure risk in this cohort. These findings are exploratory and hypothesis-generating, and external validation and calibration are required before any routine clinical or decision-support use.