JSS Academy of Higher Education & Research, formerly Jagadguru Sri Shivarathreeshwara University or JSS University, is an institute of higher education deemed to be university located in Mysore, Karnataka, India. It was established in 2008 and is part of JSS Mahavidyapeetha, which runs a variety of educational institutions. JSS Academy of Higher Education & Research is focused on medical and health-related studies, and comprises of JSS Medical College, JSS Dental College and Hospital and JSS College of Pharmacy at the main campus in Mysore as well as JSS College of Pharmacy in Ootacamund, in the neighbouring state of Tamil Nadu.
The aspiration of this review is to discuss the intricate development of Müller glial cells (MGCs) and their indispensable neuroprotective and regenerative roles, as well as novel avenues of treatment for retinal neurodegenerative diseases. MGCs are the principal radial glial cells of the vertebrate retina, extending from what is composed of a characteristic funnel-shaped morphology spanning throughout the retinal thickness. Their cell bodies are in the inner nuclear layer (INL), and their processes span from the outer limiting membrane to the inner limiting membrane, where they strongly associate with neurons, blood vessels, and the extracellular matrix across all layers of retinal structure. These cells preserve ionic and water homeostasis, control neurotransmitter uptake, and participate in constructing the blood retinal barrier (BRB), as well as deliver crucial metabolic help to neurons by means of the glutamate-glutamine cycle, thus excluding excitotoxic injury. First, we analysed the molecular processes underlying MGCs activation: pro-inflammatory molecules, Reactive oxygen species (ROS), and survival pathways. Special notice was made of changes in gene expression upon activation and the recrudescence of embryonic developmental programs that permit cell-cycle re-entry and retinal regeneration. Systematic searches of Google Scholar and PubMed to find relevant literature. Upon activation, Müller’s glia, a type of retinal support cell, commence the expression of protective genes, such as Zfp36, Mt1, and Slc14a1. Some creatures could regenerate; however, in mammals, this capacity is limited, which is particularly evident in the retina, where, despite the activation of Müller’s glia, full regeneration of damaged photoreceptors is not achieved. MGCs produces retinal progenitors that assist photoreceptors and interneurons while maintaining retinal integrity. MGCs contain progenitor cells that can differentiate into both neurons and other retinal cell types. Molecular targets for retinal therapeutics that utilize MGCs include pathways that regulate inflammation and oxidative stress. Müller glial cells are essential for maintaining retinal health, safeguarding neurons, and facilitating their regeneration. Targeted molecular therapy is addressed as a promising strategy for retinal neurodegenerative diseases, using their regenerative and protective potential.
Urolithin A (UA) is synthesized when the body metabolizes ellagic acid and ellagitannins. UA has been a widely recognized physiologically active compound throughout the previous decade. The gut microbiota affects metabolic regulators AMPK and sirtuins, initiates autophagy, and activates mitochondrial quality control, which is essential for infection resistance, intestinal health, and inflammation reduction. A preclinical study indicates that UA alters cancer cell metabolism, fortifies the intestinal barrier, safeguards the brain, and supports skeletal muscle health. UA enhances muscle endurance, mitochondrial function indicators, and cardiometabolic health without side effects or adverse reactions in preliminary human trials, primarily including the elderly and sedentary individuals. UA production exhibits significant variability due to the heterogeneity of gut flora. The existing classifications of A, B, and O kinds, absence of longitudinal data, limited trial sizes, and inconsistency between results and real-world outcomes impede the pharmaceutical advancement of UA. This review commenced with an examination of UA’s origins, chemical properties, gastrointestinal metabolism, absorption, molecular functions, and therapeutic potential. The literature’s validity, applicability, and knowledge gaps indicate that UA is a postbiotic treatment that influences the gut microbiome’s impact on mitochondrial pathways affecting various bodily systems, considering the intricate connections among inflammation, aging, and cancer. Comprehensive clinical trials are required to validate the optimal composition, dosage, and therapeutic efficacy. Dietary ellagitannins, the gut microbial transformation to urolithin A, and its systemic mitochondrial and therapeutic advantages
Piper longum Linn (P. longum), a historically revered culinary spice and medicinal herb, has transitioned from its traditional roots in Ayurveda, Siddha, and Unani medicine to modern biomedical and technological applications. This review provides a comprehensive overview of its phytochemistry, therapeutic potential, and translational relevance in drug development. Rich in bioactive compounds such as piperine, piperlongumine, and piperlonguminine, P. longum exhibits significant antimicrobial, antioxidant, anti-inflammatory, cardioprotective, antidiabetic, and anticancer activities. Emerging studies also highlight its role as a bioenhancer, functional food ingredient, and sustainable source for nutraceuticals. Furthermore, advances in nanotechnology including liposomes, cubosomes, and transgelosomes, have enhanced its solubility, bioavailability, and targeted pharmacological efficacy. Industrial applications span nutraceuticals, phytopharmaceuticals, and green nanotechnology, underscoring its potential for commercialization. Clinical and preclinical studies validate its efficacy and safety within therapeutic ranges. By bridging ancient knowledge with modern innovations, this review highlights P. longum as a versatile candidate for integrative medicine and novel drug delivery strategies.
Biopolymer hydrogel-based nanocomposites functionalized with natural products have emerged as advanced therapeutic platforms for next-generation wound dressings, addressing the multifactorial challenges associated with acute and chronic wounds. By integrating biocompatible hydrogel scaffolds with natural product-derived bioactives and nanoparticle-enabled delivery systems, these multifunctional constructs provide a moist wound microenvironment, promote gas exchange, regulate exudates, and support cellular adhesion, proliferation, and tissue regeneration. This review critically examines recent advances in the design, fabrication, and functionalization of biopolymer hydrogels with natural product-based nanoparticles, highlighting their synergistic roles in enhancing antimicrobial efficacy, antioxidant defense, anti-inflammatory responses, angiogenesis, and controlled drug release. Key structure-property-function relationships are discussed, with emphasis on hydrogel composition, crosslinking strategies, physicomechanical performance, and release kinetics in relation to wound healing outcomes. Furthermore, emerging technologies such as bioinspired nanocomposites, smart and stimuli-responsive hydrogels, and advanced fabrication approaches are evaluated. Importantly, translational considerations including scalability, sterilization, batch-to-batch consistency, regulatory pathways, and available preclinical and clinical evidence are addressed to bridge laboratory research with clinical implementation. Collectively, this review underscores natural product-functionalized biopolymer hydrogel nanocomposites as a promising, sustainable, and patient-centric strategy for therapeutic wound care and translational drug design and development.
Ischemic stroke remains a major global health burden, with secondary mechanisms of injury playing a critical role in initiation and progression of long-term neurological outcomes. Among these, the formation of neutrophil extracellular traps (NETosis) has gained significant traction as a key process that links innate immune activation with thrombotic and inflammatory damage in stroke. Shortly after the onset of cerebral ischemia, neutrophils rapidly infiltrate the affected tissue and undergo NETosis in response to Damage Associated Molecular Pattern (DAMPs) and inflammatory cues, releasing NET structures that interact with platelets, endothelial cells, and coagulation pathways. These NET components promote thrombus formation, enhance its structural stability, and confer resistance to fibrinolytic therapies, all while aggravating blood-brain barrier (BBB) breakdown, neuronal injury, and downstream neuroinflammatory cascades disturbing gut-brain axis and post stroke recovery. Clinical and pre-clinical investigations have shown that NET-related markers such as citrullinated histone H3, Myeloperoxidase (MPO)-DNA complexes, and circulating cell-free DNA are closely associated with stroke severity, infarct burden, and poorer clinical recovery, supporting their use as potential prognostic indicators. Experimental strategies aimed at inhibiting NET formation or accelerating its dissolution, including DNase-I administration, Peptidyl arginine deiminase 4 (PAD4) inhibition, and blockade of MPO activity, have demonstrated neuroprotective effects by reducing infarct size, preserving BBB function, and enhancing functional outcomes in animal models. Despite these encouraging findings, translating NET-targeted therapies into clinical practice remains complex due to the diversity of patient profiles and comorbidities that are weighing down translation efforts. This review highlights the central contribution of NETosis to stroke-related thrombosis, BBB disruption, and sustained inflammation, while emphasising the evolving potential of NET-focused interventions as future therapeutic tools in Ischemic stroke.
