Scholarly Publications
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This community showcases the academic contributions of faculty and researchers at Banaras Hindu University (BHU) and provides a year-wise compilation of publications across disciplines. Institutional Repository BHU
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PublicationBook Chapter Unraveling the complexity of chronic diseases: an introductory exploration(Elsevier, 2025) Chandrabhan Prajapati; Payal Singh; Sachchida Nand Rai; Santosh Kumar SinghChronic illnesses comprising diabetes, cardiovascular, cancerous diseases, along with depression present a major global health challenge due to their long duration, gradual onset, and often irreversible progression. These conditions can lead to severe complications, including damage to organs such as the heart and kidneys while also increasing susceptibility to infectious illnesses like coronavirus disease-2019. Noncommunicable diseases account for 74% of worldwide deaths, with 77% occurring in low as well as moderate-income countries. The economic burden of chronic diseases is also substantial, contributing to $3.8 trillion in healthcare costs yearly in the United States. The personal toll of chronic illness is significant, affecting patients’ autonomy, identity, and mental well-being, as long-term management often leads to lifestyle changes and stress. Despite the importance of primary care, most health systems remain focused on acute, episodic care, lacking the infrastructure for sustained, coordinated management. This highlights the need for healthcare policies to prioritize long-term, proactive care. Prevention, early diagnosis, and lifestyle changes are essential in reducing the impact of chronic diseases. Advances in precision medicine, polygenic risk prediction, and digital health technologies offer the potential for better detection and management, though their collective impact at the population level requires further study. In low-resource settings, the challenge of managing both chronic and communicable diseases is even more pressing. Limitations of this chapter include evolving definitions of chronic illness and the lack of comprehensive data on integrated prevention and management strategies, especially in low-income regions, underscoring the need for further research. © 2026 Elsevier Inc. All rights reserved.PublicationBook Chapter Therapeutic potential of alkaloids in treatment of gut-associated diseases(Elsevier, 2025) Falguni Goel; Aditi Giri; Vipin Kumar Garg; Payal SinghAlkaloids, a broad group of naturally occurring nitrogenous compounds, have gained universal interest due to their drug value in the treatment of gut-associated diseases. The bioactive compounds have been found to exhibit varied pharmacological activities from antiinflammatory, antioxidant, antimicrobial to gut microbiota-modulating activities. Recent reports highlight their applications in the treatment of diseases such as inflammatory bowel syndrome, inflammatory bowel disease, gastroesophageal reflux disease, and peptic ulcers by modulating key molecular targets such as NF-κB, MAPK, and Nrf2. Alkaloids berberine, piperine, sanguinarine, and quinine are found to be active in regulating gut motility, enhancing intestinal barrier function, and immune response modulation. In addition, advancements in drug delivery systems, such as nanoformulations, have also improved their bioavailability and therapeutic potential. This chapter discusses an in-depth overview of the phytochemistry, mechanisms of action, preclinical and clinical trials, and areas of future interest of alkaloids in gut health. Clarification of their molecular interactions and pharmacological properties may unlock new avenues in the treatment of gastrointestinal disorders. © 2026 Elsevier Inc. All rights reserved..PublicationArticle “Sustainable synthesis of Camellia sinensis-mediated silver nanoparticles (CsAgNP) and their anticancer mechanisms in breast cancer cells”(Elsevier Ltd, 2025) Rupen Tamang; Abhishesh Kumar Mehata; Virendra Pratap Singh; Madaswamy Sona S Muthu; Biplob KochThe present investigation focuses on synthesizing eco-friendly and cost-effective silver nanoparticles (CsAgNP) utilizing Camellia sinensis ethanolic extract (CsE) as a reducing agent and investigating the potential enhancement in its anticancer efficacy as compared to CsE. The CsAgNP formation was confirmed through the color change from pale green to dark brown and further validated using UV–visible spectroscopy in the 400-450 nm range. The optimal CsAgNP synthesis parameters include 1:4 ratio of CsE: 1 mM AgNO3, 60 min of duration and 50 °C reaction temperature. The morphology and the size of nanoparticles were estimated using AFM, SEM and TEM where the results showed a smooth topography with a size <100 nm. The CsAgNP crystalline form was confirmed through SAED pictures and silver's presence confirmed through EDX analysis. FTIR study ascertained the capping agents and distortion in functional groups compared to CsE. The anticancer potency of CsAgNP and crude extract (CsE) was assessed against the T-47D breast cancer cells by MTT assay. CsAgNP displayed strong activity towards T-47D cells (IC50 8 μg/ml) compared to CsE and relatively low activity towards the normal HEK-293 cells. Further, fluorescence microscopy and flow cytometry data revealed that the CsAgNP promotes apoptosis and also induces G2-M phase cell cycle arrest. Furthermore, CsAgNP treatment decreases p53 and Bcl-2 protein expression, while increasing Bax, Cytochrome c and Caspase-3 levels, indicating mitochondrial-mediated apoptotic pathway activation. Thus, our research aims to investigate the potential of using Camellia sinensis to synthesize CsAgNP, a potent drug delivery system, to enhance anticancer effectiveness and advance cancer therapy in the future. © 2024 Elsevier B.V.PublicationArticle In vivo, in vitro, and in silico approaches in the detailed study of di-butyl phthalate (DBP), a plasticizer-induced lung fibrosis via Nrf-2/Keap-1/HO-1 pathway and its regulation(Academic Press Inc., 2025) Payal Singh; Sneha Kumari; Harshika Chakravortty; Ajai Kumar Pandey; Debabrata Dash; Rashmi N. SinghThe alveolar epithelium is a crucial barrier against external threats, yet it becomes a key player in initiating pulmonary fibrosis when compromised. Despite its importance, the intricate relationship between, DBP exposure and alveolar epithelial cell injury ensuing pro-fibrotic effects remains poorly understood. Phthalates, ubiquitous in nature, pose a significant risk to lung health upon inhalation, acting as immune triggers that cause airway inflammation and epithelial damage. We aimed to investigate the impact of intranasal administration of Di-butyl Phthalate (DBP) inhalation, and its probable effects on normal and asthmatic lungs. DBP was administered via intranasal route in normal and OVA-induced asthmatic mice. DBP exposure enhanced oxidative stress and inflammatory parameters, leading to exacerbated asthmatic response and oxidative lung damage. Enhanced accumulation of immune cells, bronchial thickening, and collagen deposition was noted in histopathological investigations of DBP-exposed lung sections. Curcumin, a plant-derived molecule, significantly mitigated DBP-exposed asthma exacerbations by suppressing NF-κB expression and enhancing NRF2 levels via the Nrf-2/Keap-1/HO-1 signaling pathway. FACS analysis revealed increased CD11b+ cells (32 %) in asthmatic mice which were reduced in the curcumin pre-treatment group (10.5 %). Enhanced epithelial to mesenchymal transition (EMT) was noted in mice lungs and A549 cells where E-cadherin expression was reduced as compared to Vimentin, and α-SMA. Apart from aggravated airway inflammation, DBP exposure damages healthy lungs also. MMP-9/TIMP-1 ratios and collagen-1 levels were restored which were enhanced after DBP exposure. Moreover, antioxidant enzyme levels such as NQO-1, HO-1, and Catalase were significantly enhanced (p < 0.01) and comparable to dexamethasone, a conventional corticosteroid. Notably, both dexamethasone and curcumin treatments effectively regulated the stimulation and accumulation of Nrf-2 in the nucleus, promoting antioxidant production and offering potential therapeutic benefits in mitigating pulmonary fibrosis. OVA and DBP alone caused DNA damage in the lung cells where increased percentage of damaged DNA movement in the tail, tail length, tail moment, and olive tail moment indicated severe damage in the DBP and OVA combined exposure strategies. Dexamethasone and Curcumin treatments reduced the extent of the DNA damage indicating anti-inflammatory and ant-oxidative potentials. Moreover, in silico studies are supportive of therapeutic potential of Curcumin and Dexamethasone in DBP-induced lung inflammation and fibrosis. © 2024 Elsevier Inc.PublicationArticle Intracellular reactive oxygen species scavenging potential of Benincasa hispida Cogn. confection(National Institute of Science Communication and Policy Research, 2025) Kalpana Patni; Praveen P. Kumar; Sristi Pandey; Birinchi Kumar Sarma; Neha GargUnchecked levels of Reactive Oxygen Species (ROS) are known contributors in numerous health issues like metabolic disorders, neurological disorders and cancers. A traditional herbal preparation, Benincasa hispida Confection (BHC) is hypothesized to balance the levels ROS because of the presence of inherent antioxidative phytocomponents. However, the specific mechanisms underlying BHC purported ROS scavenging effects at cellular level have remained unexplored. We prepared BHC, and profiled its antioxidative molecules through HPLC analysis. Preparation method included B. hispida pulp base mixed with sugar candy and various medicinal herbs as key ingredients to enhance its taste and palatability. The ability to scavenge intracellular ROS was investigated using 2',7'-dichlorofluorescin-diacetate (DCF-DA) assay after ensuring the cell viability upon treatment with the extract of BHC. BHC was rich in previously known antioxidant molecules and was able to quench intracellular ROS. B. hispida also contributed to its ROS quenching abilities along with other ingredients. This study provides valuable insights into the therapeutic utility of BHC and advocates that consumption of BHC might protect the individuals from the ROS mediated oxidative stress and associated diseases. © 2025, National Institute of Science Communication and Policy Research. All rights reserved.PublicationArticle Chronic unpredictable stress exposure disrupts testicular function by modulating germ cell-junctional dynamics and Nrf2/HO-1/IKKβ/NF-κB pathway(Elsevier Inc., 2025) Shubhanshu Yadav; Anupam Yadav; Raghav Kumar MishraThe unpredictable nature of stress complicates understanding its relationship with male infertility. In this study, we investigated testicular germ cell and junctional dynamics in male mice following exposure to chronic unpredictable stress (CUS). Adult Parkes male mice were exposed to CUS for 35 days (one complete spermatogenic cycle), with a random stressor (restraint stress, water deprivation, food deprivation, light flashing, wet bedding, cage shaking, or cage tilting) applied once per day in an intermittent and unpredictable manner to avoid repeating the same stimulus on consecutive days. CUS exposure caused behavioral alterations in mice, as observed through the forced swim test and the tail suspension test. CUS inhibited testosterone biosynthesis by decreasing steroidogenic markers (SF-1, StAR, 3β-HSD, and 17β-HSD). It also resulted in altered oxido-inflammatory and apoptotic markers, including increased LPO, Caspase-3, IKKβ, and NF-κB, along with decreased Nrf2, HO-1, SOD, and catalase in the testis. CUS exposure reduced 1 C and 4 C germ cell populations and decreased germ cell ratios (1 C:2 C, 4 C:2 C, and 4 C:S-phase), impairing sperm development. CUS disrupted meiosis initiation, chromosomal synapsis, and germ cell maintenance by reducing Stra8, SYCP3, and Piwil1 expression in the testis. It also adversely affected blood-testis barrier markers, such as ZO-1 and connexin43. These changes led to altered testicular histomorphology, reduced daily sperm production, and disrupted germ cell dynamics. The findings suggest that CUS inhibits steroidogenesis and perturbs the Nrf2/HO-1/IKKβ/NF-κB oxido-inflammatory pathway. This leads to disrupted germ cell dynamics, compromised blood-testis barrier integrity, altered histomorphology, and reduced sperm production, collectively resulting in testicular dysfunction. © 2025 Elsevier Inc.PublicationArticle TCE-mediated neuroprotection against rotenone-induced dopaminergic neuronal death in PD mice: insights into the Nrf-2/PINK1/Parkin-mitophagy pathway(Springer, 2025) Hagera Dilnashin; Shekhar Singh; Poonam Rawat; Aaina Singh Singh Rathore; Richa S. Singh; Priyanka Kumari Keshri; Nitesh Kumar Gupta; Singh Ankit Satyaprakash; Surya Pratap SinghOxidative stress-induced mitochondrial dysfunction is implicated in the pathogenesis of Parkinson’s disease (PD). In a previous study, we reported that an extract of T. cordifolia (TCE) possessed antioxidant and anti-apoptotic properties that improved mitochondrial function against rotenone-induced neurotoxicity. However, the underlying molecular mechanism remains unclear. In this study, we found that rotenone (ROT)-induced PD mice exhibited mitochondrial abnormalities, including defective mitophagy, mitochondrial reactive oxygen species (ROS) overexpression, and mitochondrial fragmentation, accompanied by reduced expression of Pink1 and Parkin and increased apoptosis. These changes were partially reversed following oral administration of TCE. Moreover, TCE restored the activity and translocation of NF-E2-related factor 2 (Nrf2) and upregulated the expression of antioxidant enzymes (SOD1, SOD2, GSH, and GSSH). Interestingly, ROT also activates mitophagy. Our results suggest that ROT toxicity can cause neuronal cell death through mitophagy-mediated signaling in PD mice. However, TCE reversed this activity by inhibiting autophagic protein (LC3B-II/LC3B-I) activation and increasing specific mitochondrial proteins (TOM20, Pink1, and Parkin). Our findings indicated that TCE provides neuroprotection against rotenone-induced toxicity in PD mice by stimulating endogenous antioxidant enzymes and inhibiting ROT-induced oxidative stress by potentiating the Nrf-2/Pink1/Parkin-mediated survival mechanism. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2025.PublicationArticle Chlorogenic acid, a dietary phenolic acid ameliorates hepatorenal injury in streptozotocin-induced diabetic rats through regulation of oxidative stress and inflammation(Elsevier Ltd, 2025) Amit Kumar Singh; Harvesh Kumar Rana; Rohit Sharma; Abhay K. PandeyDiabetes is commonly associated with oxidative stress, a factor believed to contribute in its development and progression. Chlorogenic acid (CGA), a phenolic compound found in coffee and other food sources has been shown to have antioxidant and anti-inflammatory properties by scavenging free radicals. In the present study, CGA was assessed for its ability to reduce oxidative stress in the liver and kidney, as well as serum inflammatory response in streptozotocin (STZ)-induced diabetic rats. STZ (50 mg/kg)was administered intraperitoneally to male albino Wistar rats to induce experimental diabetes and were divided into five groups (n = 5); control, diabetic control, diabetic/metformin-treated, diabetic/CGA (100 and 150 mg/kg) treated. Diabetic rats showed significant elevation in pro-inflammatory cytokines (TNF-α, IL-6, and IFN-γ) and decreased concentration of the anti-inflammatory cytokine IL-10. They also had reduced activity of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), and reduced glutathione (GSH), as well as increased levels of peroxidation marker in their liver and kidney tissues when compared to control rats. Oral administration of CGA (100 and 150 mg) for 28 days markedly (p < 0.05) improved all of these inflammatory and oxidative stress parameters in diabetic rats. These findings were further corroborated through histopathological examination of hepatic and renal tissues. The observed results indicate that CGApossess antioxidant and anti-inflammatory property, as evidenced by reduction in redox imbalance, inflammation and lipid peroxidation to near normal, thus offering protection to the liver and kidneys tissues from damage inflicted due to oxidative stress and inflammation in diabetic rats. © 2025 Elsevier LtdPublicationArticle The ability of low levels of elevated ozone to change the growth and phytochemical constituents of a medicinal plant Andrographis paniculata (Burm. f.) Nees(Springer, 2025) Naushad Ansari; Durgesh Singh Yadav; Priyanka K. Singh; Madhoolika Agrawal; Shahibhushan AgrawalGround-level ozone (O3) is well recognized as a secondary air pollutant with detrimental effects on plant growth and biochemistry. In a field study, Andrographis paniculata (King of Bitter) was exposed to ambient O3 and elevated O3 (AO + 20 ppb) at three growth stages [45, 90, and 135 days after treatment, (DAT)] using open-top chambers. Elevated O3 stress negatively impacted plant growth, increased cell damage, and induced foliar injuries. However, elevated O3 also boosted antioxidant production such as proline, phenol, and enzymatic antioxidants, as well as certain secondary metabolites such as tannins, phytosterols, saponins, and alkaloids. This may enhance the plant's medicinal properties, including compounds limonene dioxide, phytol, palmitic acid, and androstadiene. While, certain metabolites like Citronellol, Khusenol, and tocopherol displayed an adverse reaction under elevated O3 exposure. The novel detection of acrodiene, squalene, and neophytadiene under O3 stress emphasizes their medicinal significance. Notably, an important bioactive compound andrographolide in A. paniculata showed increased synthesis under elevated O3 at 45 and 90 DAT, suggesting that O3 exposure could enhance the plant's pharmaceutical value. © The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, part of Springer Nature 2024.PublicationArticle Contrasting effects of melatonin on Brassica juncea and Alternaria brassicae reduce pathogenicity of the fungus and alleviate damage to plants(Elsevier B.V., 2025) Anchal Garg; Sujit Shah; Tirth Bhargav Bhai Patel; Vibhav Gautam; Deepak KumarBrassica juncea (Indian mustard) is a vital oil seed crop in India and is grown worldwide for oil and food requirements. Alternaria brassicae is a major threat to B. juncea quality and productivity causing worldwide crop loss. In this work, it was observed that exogenous melatonin (MT) at 200 µM concentration was proven to be well effective against A. brassicae, which reduced disease consequences up to 75 %, attributed to significant reduction of necrotic lesions, delayed onset infection, and improved plant defence by enhancing chlorophyll and proline content, maintaining water retention and reducing oxidative stress. Additionally, biochemical assays, such as reduced oxidative damage, as evidenced by diminished levels of malondialdehyde (MDA), hydrogen peroxide (H2O2) and enhanced antioxidant enzyme activities, clearly showed the antifungal effect of MT on Alternaria. This study represents a new insight into the potential role as sustainable antifungal compound. Furthermore, HRMS metabolite profiling of A. brassicae cultured with MT revealed altered fungal metabolite profiles, including increased production of known antifungal compounds, suggesting that MT disrupts fungal metabolism and reduces its pathogenicity. In contrast, a decrease in the levels of antioxidant and indole derivatives in fungal extracts indicated weaker fungal defenses. The major aim of the study to provide evidence for the curative potential of MT as an effective antifungal molecule against A. brassicae in B. juncea that would be beneficial to agricultural improvement and an eco-friendly alternative to chemical fungicides. © 2025