Dr. Pranesh Kumar
@lkouniv.ac.in
Assistant Professor, Institute of Pharmaceutical Sciences
University of Lucknow, Lucknow
Dr. Pranesh Kumar working as Assistant Professor in Aryakul College of Pharmacy & Research, Lucknow. He completed B. Pharm from PSIT Kanpur and qualified GATE/GPAT. Further M. Pharm from BBAU Lucknow (A Central University) and awarded by Double Gold medal. Again completed Ph.D. in Pharmacology from BBAU Lucknow (A Central University) and got DST INSPIRE fellowship (JRF & SRF). His research expertise in Anti-Cancer, Nanoformulations, In silico, In vitro and In vivo Drug Design, NMR metabolomics.
EDUCATION
M.Pharm, Ph.D.
RESEARCH INTERESTS
Research expertise in Anti-Cancer, Nanoformulations, In silico, In vitro and In vivo Drug Design, NMR metabolomics.
Scopus Publications
Scholar Citations
Scholar h-index
Scholar i10-index
Scopus Publications
Archana Bharti Sonkar, Pranesh Kumar, Anand Kumar, Anurag Kumar Gautam, Abhishek Verma, Amita Singh, Umesh Kumar, Dinesh Kumar, Tarun Mahata, Bolay Bhattacharya,et al.
Elsevier BV
Sahin Reja, Kaushik Sarkar, Deboshmita Mukherjee, T.K.S. Fayaz, Pranesh Kumar, Purak Das, Palash Sanphui, and Rajesh Kumar Das
Elsevier BV
Madhuri Basak, Abhishek Singh Sengar, Kiran Das, Tarun Mahata, Manish Kumar, Dinesh Kumar, Sayan Biswas, Subhasish Sarkar, Pranesh Kumar, Priyadip Das,et al.
Proceedings of the National Academy of Sciences
Dose-limiting cardiotoxicity remains a major limitation in the clinical use of cancer chemotherapeutics. Here, we describe a role for Regulator of G protein Signaling 7 (RGS7) in chemotherapy-dependent heart damage, the demonstration for a functional role of RGS7 outside of the nervous system and retina. Though expressed at low levels basally, we observed robust up-regulation of RGS7 in the human and murine myocardium following chemotherapy exposure. In ventricular cardiomyocytes (VCM), RGS7 forms a complex with Ca 2+ /calmodulin-dependent protein kinase (CaMKII) supported by key residues (K412 and P391) in the RGS domain of RGS7. In VCM treated with chemotherapeutic drugs, RGS7 facilitates CaMKII oxidation and phosphorylation and CaMKII-dependent oxidative stress, mitochondrial dysfunction, and apoptosis. Cardiac-specific RGS7 knockdown protected the heart against chemotherapy-dependent oxidative stress, fibrosis, and myocyte loss and improved left ventricular function in mice treated with doxorubicin. Conversely, RGS7 overexpression induced fibrosis, reactive oxygen species generation, and cell death in the murine myocardium that were mitigated following CaMKII inhibition. RGS7 also drives production and release of the cardiokine neuregulin-1, which facilitates paracrine communication between VCM and neighboring vascular endothelial cells (EC), a maladaptive mechanism contributing to VCM dysfunction in the failing heart. Importantly, while RGS7 was both necessary and sufficient to facilitate chemotherapy-dependent cytotoxicity in VCM, RGS7 is dispensable for the cancer-killing actions of these same drugs. These selective myocyte-intrinsic and myocyte-extrinsic actions of RGS7 in heart identify RGS7 as an attractive therapeutic target in the mitigation of chemotherapy-driven cardiotoxicity.
Sudipta Saha, Amita Singh, Pranesh Kumar, Archana Bharti Sonkar, Anurag Kumar Gautam, Abhishek Verma, Biswanath Maity, Himani Tiwari, Nanda Gopal Sahoo, Amit K. Keshari,et al.
Bentham Science Publishers Ltd.
PCSK9 is a strongly expressed protein in the liver and brain that binds to the LDLR and regulates cholesterol in the liver effectively. Other receptors with which it interacts include VLDLR, LRP1, ApoER2, and OLR1. PCSK9 gain-of-function results in lysosomal degradation of these receptors, which may result in hyperlipidemia. PCSK9 deficiency results in a lower amount of cholesterol, which reduces cholesterol's accessibility to cancer cells. PCSK9 regulates several proteins and signaling pathways in cancer, including JNK, NF-κВ, and the mitochondrial-mediated apoptotic pathway. In the liver, breast, lungs, and colon tissue, PCSK9 initiates and facilitates cancer development, while in prostate cancer cells, it induces apoptosis. PCSK9 has a significant impact on brain cancer, promoting cancer cell survival by manipulating the mitochondrial apoptotic pathway and exhibiting apoptotic activity in neurons by influencing the NF-κВ, JNK, and caspase-dependent pathways. The PCSK9 impact in cancer at different organs is explored in this study, as well as the targeted signaling mechanisms involved in cancer growth. As a result, these signaling mechanisms may be aimed for the development and exploration of anti-cancer drugs in the immediate future.
Deboshmita Mukherjee, Sahin Reja, Kaushik Sarkar, T.K.S. Fayaz, Pranesh Kumar, Ambica Kejriwal, Purak Das, Palash Sanphui, and Rajesh Kumar Das
Elsevier BV
Kiran Das, Madhuri Basak, Tarun Mahata, Manish Kumar, Dinesh Kumar, Sayan Biswas, Suvro Chatterjee, Mahammed Moniruzzaman, Nimai Chandra Saha, Kausik Mondal,et al.
Elsevier BV
Anurag Kumar Gautam, Pranesh Kumar, Biswanath Maity, Ganesh Routholla, Balaram Ghosh, Kumarappan Chidambaram, M. Yasmin Begum, Adel Al Fatease, P.S. Rajinikanth, Sanjay Singh,et al.
Frontiers Media SA
Hepatocellular carcinoma (HCC) is a common malignancy which affects a substantial number of individuals all over the globe. It is the third primary cause of death among persons with neoplasm and has the fifth largest mortality rate among men and the seventh highest mortality rate among women. Dalbergin (DL) is described to be effective in breast cancer via changing mRNA levels of apoptosis-related proteins. DL belongs to neoflavonoids, a drug category with low solubility and poor bioavailability. We created a synthetic version of this naturally occurring chemical, DL, and then analyzed it using 1H-NMR, 13C-NMR, and LC-MS. We also made PLGA nanoparticles and then coated them with galactose. The design of experiment software was used to optimize DL-loaded galactose-modified PLGA nanoparticles. The optimized DL-nanoformulations (DLF) and DL-modified nanoformulations (DLMF) were analyzed for particle size, polydispersity index, shape, and potential interactions. In-vitro experiments on liver cancer cell lines (HepG2) are used to validate the anti-proliferative efficacy of the modified DLMF. The in-vitro research on HepG2 cell lines also demonstrated cellular accumulation of DLF and DLMF by FITC level. The in-vitro result suggested that DLMF has high therapeutic effectiveness against HCC. In-vivo pharmacokinetics and bio-distribution experiments revealed that DLMF excelled pristine DL in terms of pharmacokinetic performance and targeted delivery, which is related to galactose’s targeting activity on the asialoglycoprotein receptor (ASGPR) in hepatic cells. Additionally, we performed an in-silico study of DL on caspase 3 and 9 proteins, and the results were found to be −6.7 kcal/mol and −6.6 kcal/mol, respectively. Our in-silico analysis revealed that the DL had strong apoptotic properties against HCC.
Raquibun Nisha, Pranesh Kumar, Umesh Kumar, Nidhi Mishra, Priyanka Maurya, Priya Singh, Heena Tabassum, Alka, Samipta Singh, Anupam Guleria,et al.
Elsevier BV
Archana Sonkar, Pranesh Kumar, Anurag Gautam, Biswanath Maity, and Sudipta Saha
Bentham Science Publishers Ltd.
: Lung Cancer (LC) is the leading cause of cancer deaths worldwide. Recent research has also shown LC as a genomic disease, causing somatic mutations in the patients. Tests related to mutational analysis and genome profiles have lately expanded significantly in the genetics/genomics field of LC. This review summarizes the current knowledge about different signalling pathways of LC based on the clinical impact of molecular targets. It describes the main molecular pathways and changes involved in the development, progression, and cellular breakdown of LC and molecular changes. This review focuses on approved and targeted experimental therapies such as immunotherapy and clinical trials that examine the different targeted approaches to treating LC. We aim to clarify the differences in the extent of various genetic mutations in DNA for LC patients. Targeted molecular therapies for LC can be continued with advanced racial differences in genetic changes, which have a significant impact on the choice of drug treatment and our understanding of the profile of drug susceptibility/ resistance. The most relevant genes described in this review are EGFR, KRAS, MET, BRAF, PIK3CA, STK11, ERBB3, PTEN, and RB1. Combined research efforts in this field are required to understand the genetic difference in LC outcomes in the future.
Anurag Kumar Gautam, Pranesh Kumar, Ritu Raj, Dinesh Kumar, Bolay Bhattacharya, P.S. Rajinikanth, Kumarappan Chidambaram, Tarun Mahata, Biswanath Maity, and Sudipta Saha
Frontiers Media SA
Hepatocellular carcinoma (HCC) is one of the most common tumors affecting a large population worldwide, with the fifth and seventh greatest mortality rates among men and women, respectively, and the third prime cause of mortality among cancer victims. Dimethyl itaconate (DI) has been reported to be efficacious in colorectal cancer by decreasing IL-1β release from intestinal epithelial cells. In this study, diethylnitrosamine (DEN)-induced HCC in male albino Wistar rats was treated with DI as an anticancer drug. The function and molecular mechanism of DI against HCC in vivo were assessed using histopathology, enzyme-linked immunosorbent assay (ELISA), and Western blot studies. Metabolomics using 1H-NMR was used to investigate metabolic profiles. As per molecular insights, DI has the ability to trigger mitochondrial apoptosis through iNOS- and eNOS-induced activation of the NF-κB/Bcl-2 family of proteins, CytC, caspase-3, and caspase-9 signaling cascade. Serum metabolomics investigations using 1H-NMR revealed that aberrant metabolites in DEN-induced HCC rats were restored to normal following DI therapy. Furthermore, our data revealed that the DI worked as an anti-HCC agent. The anticancer activity of DI was shown to be equivalent to that of the commercial chemotherapeutic drug 5-fluorouracil.
Pranesh Kumar, Mohit Kumar, Anurag Kumar Gautam, Archana Bharti Sonkar, Abhishek Verma, Amita Singh, Raquibun Nisha, Umesh Kumar, Dinesh Kumar, Tarun Mahata,et al.
Elsevier BV
Pranesh Kumar, Anurag Kumar Gautam, Umesh Kumar, Archana S. Bhadauria, Ashok K. Singh, Dinesh Kumar, Tarun Mahata, Biswanath Maity, Hriday Bera, and Sudipta Saha
Informa UK Limited
Abstract The effectiveness of betulinic acid (B) and PLGA loaded nanoparticles of B (Bnp) against hepatocellular carcinoma (HCC) was established and reported earlier. In continuation of our previous report, the present study described the molecular mechanisms of their antineoplastic responses. In this context, the antineoplastic properties of both B and Bnp were evaluated on DEN-induced HCC rat model. The quantitative real-time polymerase chain reaction and western blot analyses revealed that HCC was developed through lower expressions of e-NOS, BAX, BAD, Cyt C and higher expressions of i-NOS, Bcl-xl, Bcl-2. B and Bnp normalised the expressions of these apoptogenic markers. Particularly, both activated i-NOS and e-NOS mediated Bcl-2 family proteins→CytC→Caspase 3 and 9 signalling cascades. The 1H-NMR-based metabolomics study also demonstrated that the perturbed metabolites in DEN-induced rat serum restored to the normal level following both treatments. Moreover, the antineoplastic potential of Bnp was found to be comparable with the marketed product, 5-flurouracil.
Poonam Parashar, Ifrah Mazhar, Jovita Kanoujia, Abhishek Yadav, Pranesh Kumar, Shubhini A. Saraf, and Sudipta Saha
Informa UK Limited
Abstract Present study is aimed at transdermal delivery of colchicine-loaded chitosan nanoparticles. The nanoformulations were prepared utilising spontaneous emulsification method and optimised through 23 factorial designs. The optimised formulation (CHNP-OPT) displayed an average particle size of 294 ± 3.75 nm, entrapment efficiency 92.89 ± 1.1% and drug content 83.45 ± 2.5%, respectively. In vitro release study demonstrated 89.34 ± 2.90% release over a period of 24 h. Further, CHNP-OPT incorporated into HPMC-E4M (hydroxypropyl methylcellulose) to form transdermal gel. CHNPgel displayed 74.65 ± 1.90% permeation and stability over a period of 90 days. The anti-gout potential of CHNPgel formulation was evaluated in vivo against monosodium urate (MSU) crystal-induced gout in animal model. There was significant reduction in uric acid level, during MSU administration, when compared with the conventional gel of colchicine. The enhanced therapeutic potential was witnessed through X-ray. The study revealed that colchicine-loaded CHNPgel proved their supremacy over plain colchicine and can be an efficient delivery system for gout treatment.
Sahin Reja, Deboshmita Mukherjee, Purak Das, Pranesh Kumar, and Rajesh Kumar Das
Elsevier BV
Arnab Pramanick, Sreemoyee Chakraborti, Tarun Mahata, Madhuri Basak, Kiran Das, Sumit Kumar Verma, Abhishek Singh Sengar, Praveen Kumar Singh, Pranesh Kumar, Bolay Bhattacharya,et al.
Elsevier BV
Raquibun Nisha, Pranesh Kumar, Umesh Kumar, Nidhi Mishra, Priyanka Maurya, Samipta Singh, Priya Singh, Anupam Guleria, Sudipta Saha, and Shubhini A Saraf
American Chemical Society (ACS)
Hepatocellular carcinoma (HCC) is a major cause of concern as it has substantial morbidity associated with it. Previous reports have ascertained the antiproliferative activity of imatinib mesylate (IMS) against diverse types of carcinomas, but limited bioavailability has also been reported. The present study envisaged optimized IMS-loaded lactoferrin (LF)-modified PEGylated liquid crystalline nanoparticles (IMS-LF-LCNPs) for effective therapy of IMS to HCC via asialoglycoprotein receptor (ASGPR) targeting. Results displayed that IMS-LF-LCNPs presented an optimum particle size of 120.40 ± 2.75 nm, a zeta potential of +12.5 ± 0.23 mV, and 73.94 ± 2.69% release. High-resolution transmission electron microscopy and atomic force microscopy were used to confirm the surface architecture of IMS-LF-LCNPs. The results of cytotoxicity and 4,6-diamidino-2-phenylindole revealed that IMS-LF-LCNPs had the highest growth inhibition and significant apoptotic effects. Pharmacokinetics and biodistribution studies showed that IMS-LF-LCNPs have superior pharmacokinetic performance and targeted delivery compared to IMS-LCNPs and plain IMS, which was attributed to the targeting action of LF that targets the ASGPR in hepatic cells. Next, our in vivo experiment established that the HCC environment existed due to suppression of BAX, cyt c, BAD, e-NOS, and caspase (3 and 9) genes, which thus owed upstream expression of Bcl-xl, iNOS, and Bcl-2 genes. The excellent therapeutic potential of IMS-LF-LCNPs began the significant stimulation of caspase-mediated apoptotic signals accountable for its anti-HCC prospect. 1H nuclear magnetic resonance (serum) metabolomics revealed that IMS-LF-LCNPs are capable of regulating the disturbed levels of metabolites linked to HCC triggered through N-nitrosodiethylamine. Therefore, IMS-LF-LCNPs are a potentially effective formulation against HCC.
Poonam Parashar, Pranesh Kumar, Anurag Kumar Gautam, Neelu Singh, Hriday Bera, Srimanta Sarkar, Shubhini A. Saraf, and Sudipta Saha
Elsevier
Siddhartha Maity, Sudipta Saha, Srimanta Sarkar, Pranesh Kumar, Anurag Kumar Gautam, and Archana Bharti Sonkar
Elsevier
Ashok K. Singh, Archana S. Bhadauria, Umesh Kumar, Vinit Raj, Amit Rai, Pranesh Kumar, Amit K. Keshari, Dinesh Kumar, Biswanath Maity, Sneha Nath,et al.
Springer Science and Business Media LLC
An amendment to this paper has been published and can be accessed via a link at the top of the paper.
Madhuri Basak, Tarun Mahata, Sreemoyee Chakraborti, Pranesh Kumar, Bolay Bhattacharya, Sandip Kumar Bandyopadhyay, Madhusudan Das, Adele Stewart, Sudipta Saha, and Biswanath Maity
Mary Ann Liebert Inc
AIMS
Non-steroidal anti-inflammatory drugs (NSAIDs), amongst the most commonly used drugs worldwide, are associated with gastrointestinal complications that severely limit the clinical utility of this essential class of pain medications. Here, we mechanistically dissect the protective impact of a natural product, malabaricone C, on NSAID-induced gastropathy.
RESULTS
Malabaricone C dose dependently diminished erosion of the stomach lining and inflammation in mice treated with NSAIDs with the protective impact translating to improvement in survival. By decreasing oxidative and nitrative stress, malabaricone C treatment prevented NSAID-induced mitochondrial dysfunction and cell death; NF-κB induction, release of pro-inflammatory cytokines and neutrophil infiltration; and disruptions in the vascular endothelial growth factor/endostatin balance that contributes to mucosal auto-healing. Importantly, malabaricone C failed to impact the therapeutic anti-inflammatory properties of multiple NSAIDs in a model of acute inflammation. In all assays tested, malabaricone C proved as or more efficacious than the current first line therapy for NSAID-dependent GI complications, the proton pump inhibitor omeprazole. Innovation and Conclusion: Given that omeprazole-mediated prophylaxis is, itself, associated with a shift in NSAID-driven GI complications from the upper GI to the lower GI system, there is a clear and present need for novel therapeutics aimed at ameliorating NSAID-induced gastropathy. Malabaricone C provided significant protection against NSAID-induced gastric ulcerations impacting multiple critical signaling cascades contributing to inflammation, cell loss, extracellular matrix degradation, and angiogenic auto-healing. Thus, malabaricone C represents a viable lead compound for the development of novel gastroprotective agents.
Raquibun Nisha, Pranesh Kumar, Anurag Kumar Gautam, Hriday Bera, Bolay Bhattacharya, Poonam Parashar, Shubhini A. Saraf, and Sudipta Saha
Informa UK Limited
Abstract β-sitosterol (BS), a phytosterol, exhibits ameliorative effects on hepatocellular carcinoma (HCC) due to its antioxidant activities. However, its poor aqueous solubility and negotiated bioavailability and short elimination half-life is a huge limitation for its therapeutic applications. To overcome these two shortcomings, BS-loaded niosomes were made to via, film hydration method and process parameters were optimized using a three-factor Box–Behnken design. The optimized formulation (BSF) was further surface-modified with polyethylene glycol (PEG). The resulting niosomes (BSMF) have spherical shapes, particle sizes, 219.6 ± 1.98 nm with polydispersity index (PDI) and zeta potential of 0.078 ± 0.04 and −19.54 ± 0.19 mV, respectively. The drug loading, entrapment efficiency, and drug release at 24 h of the BSMF were found to be 16.72 ± 0.09%, 78.04 ± 0.92%, and 75.10 ± 3.06%, respectively. Moreover, BSMF showed significantly greater cytotoxic potentials on Hep G2 cells with an enhanced cellular uptake relative to pure BS and BSF. The BSMF also displayed potentially improved curative property of HCC in albino wistar rat. Thus, the BSMF could be one of the promising therapeutic modalities for HCC treatment in terms of targeting potential resulting in enhanced therapeutic efficacy.
Pranesh Kumar, Aakriti Agarwal, Ashok K. Singh, Anurag Kumar Gautam, Sreemoyee Chakraborti, Umesh Kumar, Dinesh Kumar, Bolay Bhattacharya, Parthasarathi Panda, Biswajit Saha,et al.
Elsevier BV
Vimal Maurya, Pranesh Kumar, Sreemoyee Chakraborti, Ashok K. Singh, Archana S. Bhadauria, Umesh Kumar, Dinesh Kumar, Arnab Pramanik, Biswajit Saha, Venkatesh Kumar R,et al.
Elsevier BV
Vinit Raj, Archana S. Bhadauria, Ashok K. Singh, Umesh Kumar, Amit Rai, Amit K. Keshari, Pranesh Kumar, Dinesh Kumar, Biswanath Maity, Sneha Nath,et al.
Elsevier BV
P. Kumar and K. N. Rai
World Scientific Pub Co Pte Lt
In this paper, generalized dual-phase-lag (DPL) model has been studied for the numerical analysis of spatial variation of temperature within living biological tissues during thermal therapy applications. A new hybrid numerical scheme based on finite difference scheme and Chebyshev wavelet Galerkin method are used to solve the generalized DPL model with constant heat flux boundary condition. Multi-resolution and multi-scale computational property of Chebyshev wavelet in the present case localizes small scale variations of solution and fast switching of functional bases. Our study demonstrates that due to presence of coupling factor (convection–perfusion), generalized DPL model predicts lower temperature than classical DPL and Pennes model at the tumor position. Higher values of phase lag times results in lower temperature at the tumor position. But, in case of variation of phase lag time due to temperature gradient, the nature of temperature profile also depends on the spatial coordinate. The effect of the blood temperature, porosity and interfacial convective heat transfer on temperature distribution has been investigated. It is found that larger values of porosity and interfacial convective heat transfer results in lower temperature at the tumor position. Also, both porosity and interfacial convective heat transfer are pronounced more at higher values. The whole analysis is presented in dimensionless form.