ArticleCell biochemistry and biophysics2026
Polyherbal Formulation Attenuates Isoproterenol-Induced Cardiac Toxicity Through Regulation of Mitochondrial Bioenergetics, Lipid Toxicity, and Intrinsic Apoptotic Pathways in Rats.
Article in Cell biochemistry and biophysics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Isoproterenol (ISO) is a synthetic β-adrenergic agonist widely used to model xenobiotic-induced cardiac injury, primarily through mechanisms involving oxidative stress, mitochondrial dysfunction, dyslipidemia, and apoptosis. Considering the growing interest in plant-derived bioactive compounds as cardioprotective agents, this study evaluated the mechanistic potential of a polyherbal formulation (PHF) composed of Andrographis paniculata, Bauhinia variegata, Moringa oleifera, and Lantana camara. GC-MS profiling of the formulation revealed several pharmacologically relevant phytoconstituents, including 3-methylmannoside, isothiourea, L-gala-L-ido-octose, β-sitosterol, heptanal, and eicosatrienoic acid methyl ester. ISO challenge in rats resulted in pronounced cardiac injury marked by elevated biomarkers, perturbed lipid metabolism, depletion of endogenous antioxidants, mitochondrial ATP loss, Ca2+ overload, suppression of tricarboxylic acid cycle enzymes, and activation of Bax/caspase-3-mediated apoptosis. Pretreatment with PHF significantly attenuated these pathological changes by restoring antioxidant defenses, stabilizing lipid homeostasis, improving mitochondrial bioenergetics, enhancing TCA cycle activity, and modulating intrinsic apoptotic signalling. Additionally, PHF upregulated mitochondrial biogenesis mediators (PGC-1α, NRF1, TFAM) and promoted AMPK-PPARα-driven fatty acid oxidation while suppressing SREBP-1c-associated lipogenesis. Molecular docking further supported the multi-target nature of the phytochemicals through strong interactions with mitochondrial, lipid-regulatory, and apoptotic proteins. Collectively, these findings highlight the pharmacognostic value of PHF and demonstrate its potential as a natural cardioprotective intervention capable of modulating key metabolic and mitochondrial pathways involved in xenobiotic-induced cardiac toxicity.
Indexed as
Identifiers
41739316What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.