Shri Vaishnav Vidyapeeth Vishwavidyalaya

Doxorubicin, a secondary metabolite of Streptomyces peucetius var. caesius and a member of the anthracycline family, exerts anticancer effects via DNA intercalation and topoisomerase II inhibition in tumor cells. However, its clinical application is limited by dose-dependent and cumulative cardiotoxicity. The mechanisms underlying doxorubicin-induced cardiotoxicity (DIC) include oxidative stress, lipid peroxidation, mitochondrial dysfunction, calcium dysregulation, disrupted iron homeostasis, nitric oxide release, and inflammatory mediator production. Emerging evidence highlights autophagy dysregulation, with doxorubicin upregulating cardiac autophagy by suppressing GATA4 and ribosomal protein S6 kinase beta-1(S6K1). Mitochondria-dependent ferroptosis also plays a significant role, driven by downregulation of glutathione peroxidase 4 (GPX4), lipid peroxidation via DOX-Fe2+ complexes, and dysregulated iron metabolism. Additionally, DOX triggers pyroptosis in cardiomyocytes, involving proteins such as NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3), caspase-3, and gasdermin D (GSDMD). Epigenetic alterations, including DNA hypomethylation (via downregulation of DNMT1 (DNA (cytosine-5)-methyltransferase 1), changes in microRNA levels (e.g., upregulation of miR-520h targeting HDAC19 (histone deacetylase 1), and histone deacetylase inhibition, exacerbate cardiac damage. Recent studies also emphasize the role of gut microbiota in doxorubicin-induced cardiotoxicity. Doxorubicin induces dysbiosis, leading to cardiomyocyte apoptosis and elevated myocardial enzyme levels. Interventions such as dietary modifications, fecal microbiota transplantation, probiotics, and natural compounds like glabridin and emodin show promise. Glabridin reduces inflammation by modulating colonic macrophage polarization, while emodin inhibits ferroptosis via gut microbiota remodeling mediated by Nrf2. This review explores oxidative stress, lipid peroxidation, ferroptosis, apoptosis, inflammation, autophagy, epigenetics, and gut microbiota in DIC, alongside promising pharmacological strategies to mitigate its effects.

Artificial Intelligence (AI) is no longer confined to private technological innovation; it has increasingly entered the domain of governance, administration, policing, welfare distribution, and judicial decision-making in India. From predictive policing software and facial recognition systems to automated welfare eligibility tools and AI-assisted judicial research, algorithmic systems are reshaping how the State exercises power. This paper examines the emerging phenomenon of algorithmic governance in India and critically analyses its compatibility with constitutional values, administrative law principles, and the rule of law. It argues that existing Indian legal frameworks are ill-equipped to address the opacity, discretion, and accountability deficits inherent in AI-driven governance. The paper proposes a rights-centric regulatory framework rooted in constitutional morality, transparency, and human oversight. The study adopts a doctrinal and analytical methodology and draws from comparative jurisdictions to suggest reforms tailored to the Indian constitutional context.

The growing complexity and uncertainty inherent in modern information retrieval tasks necessitate systems that can reason probabilistically while leveraging rich semantic structures. This research explores the core question: How can uncertainty-aware retrieval be enhanced through the integration of probabilistic logic and knowledge graph semantics? To address this, we introduce a novel hybrid framework that fuses probabilistic soft logic (PSL) with transformer-enhanced knowledge graph embeddings (TEKGE), further empowered by a dynamic uncertainty quantification layer (DUQL). DUQL enables granular modeling of both epistemic and aleatoric uncertainties across graph entities and relationships. Additionally, a multi-hop probabilistic graph traversal (MPGT) mechanism, informed by Bayesian-regularized contextual embeddings, guides the retrieval process. Empirical evaluations on two benchmark datasets—CN15k and O*NET20k—demonstrate the system’s effectiveness, with notable gains including an 11.6

Berberine, a protoberberine isoquinoline alkaloid from Huanglian (Coptis chinensis), Huangbai (Phellodendron amurense), Huangbo (Phellodendron chinense), and Gong Lao Mu (Ilex pubescens), has been a cornerstone of Traditional Chinese Medicine for millennia, with emerging evidence supporting its multi-target pharmacology in cancer, metabolic syndrome, cardiovascular protection, and neurodegeneration. Systematic literature search of PubMed, Embase, CNKI, Wanfang, and Cochrane databases (inception–December 2025) identified preclinical/clinical studies on berberine-rich extracts or purified berberine from named botanicals, focusing on anticancer (proliferation/apoptosis), metabolic (insulin sensitization/lipogenesis), cardioprotective (anti-hypertrophic/antithrombotic), and neuroprotective (anti-amyloid/neuroinflammation) endpoints; PRISMA guidelines followed with ROBINS-I/SYRCLE quality assessment. Across 150 + studies, berberine exhibits dose-dependent efficacy that inhibits tumor growth (AMPK/mTOR, EGFR/PI3K pathways), improves glycemic/lipid control (GLP-1/GLUT4 upregulation), attenuates cardiac hypertrophy/fibrosis (AT1R/ERK signaling), and ameliorates cognitive decline (Aβ/tau clearance, gut-brain axis modulation); Huanglian extracts show superior synergy vs. isolated berberine. Multi-target network pharmacology confirmed that berberine modulates 50 + pathways (AMPK, SIRT1, Nrf2, NF-κB, gut microbiota), with botanical matrix enhancing bioavailability and mitigating toxicity; clinical trials (n > 5000) report favorable safety (GI tolerance primary limitation). Berberine's therapeutic legacy validates its repositioning across oncology, cardiometabolism, and neurology; standardized extracts from source plants offer precision polypharmacology advantages over single-target synthetics, warranting Phase III trials and pharmacognosy-guided drug discovery.

The gut–brain axis (GBA) is a bidirectional communication network integrating neural, immune, endocrine, and metabolic pathways that link the gastrointestinal tract and the central nervous system. Increasing evidence implicates gut microbiota dysbiosis in the pathogenesis of neurological disorders, including Alzheimer's disease, Parkinson's disease, multiple sclerosis, autism spectrum disorders, depression, and schizophrenia. This review synthesizes preclinical and clinical evidence to elucidate GBA-mediated mechanisms of neurological dysfunction and critically evaluates the therapeutic potential of Traditional Chinese herbal medicines (TCHMs). We highlight how dysbiosis disrupts immune signaling, microbial metabolite production, intestinal and blood–brain barrier integrity, and neurotransmitter pathways involving serotonin, dopamine, γ-aminobutyric acid, and glutamate, thereby driving neuroinflammation, oxidative stress, and neuronal injury. Particular emphasis is placed on the ability of TCHMs to restore microbial homeostasis, enhance short-chain fatty acid production, strengthen gut barrier function, and regulate neuroendocrine pathways, notably the hypothalamic–pituitary–adrenal and hypothalamic–pituitary–gonadal axes. These multi-target actions are consistently associated with improved cognitive, behavioral, and neuroinflammatory outcomes across experimental models. The review further identifies emerging synergistic strategies combining TCHMs with microbiota-targeted interventions, such as probiotics and dietary modulation, which enhance correction of dysbiosis and attenuation of neuroinflammatory cascades. Nonetheless, heterogeneity in study design, herbal formulations, and microbiome profiling limits clinical translation. Future progress will require standardized methodologies, multi-omics integration, and precision-based approaches. Overall, this review positions Chinese herbal medicines as promising systems-level modulators of the gut–brain axis for neurological disease management.