Browsing by Author "Ratan Singh Ray"

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Ambient UV-B exposure reduces the binding of ofloxacin with bacterial DNA gyrase and induces DNA damage mediated apoptosis
(Elsevier Ltd, 2016) Jyoti Singh; Ashish Dwivedi; Syed Faiz Mujtaba; Krishna P. Singh; Manish Kumar Pal; Deepti Chopra; Shruti Goyal; Ajeet K. Srivastav; Divya Dubey; Shailendra K. Gupta; Chandana Haldar; Ratan Singh Ray
Ofloxacin (OFLX) is a broad spectrum antibiotic, which generates photo-products under sunlight exposure. Previous studies have failed to explain the attenuated anti-bacterial activity of OFLX. The study was extended to explore the unknown molecular mechanism of photogenotoxicity on human skin cell line (HaCaT) under environmental UV-B irradiation. Photochemically OFLX generates ROS and caused 2′-dGuO photodegradation. We have addressed the binding affinity of OFLX and its photo-products against DNA gyrase. Significant free radical generation such as 1O2, O2•- and •OH reduces antioxidants and demonstrated the ROS mediated OFLX phototoxicity. However, the formation of micronuclei and CPDs showed photogenotoxic potential of OFLX. OFLX induced cell cycle arrest in sub-G1 peak. OFLX triggers apoptosis via permeabilization of mitochondrial membrane with the downregulation of anti-apoptotic Bcl-2 and caspase-3 whereas, upregulation of pro-apoptotic Bax and Cyto-C proteins. Our study illustrated that binding affinity of OFLX photo-products with DNA gyrase was mainly responsible for the attenuated antimicrobial activity. It was proved through molecular docking study. Thus, study suggests that sunlight exposure should avoid by drug users especially during peak hours for their safety from photosensitivity. Clinicians may guide patients regarding the safer use of photosensitive drugs during treatment. © 2016 Published by Elsevier Ltd.
Correction to: Inhibitory Effects of Bisphenol-A on Neural Stem Cells Proliferation and Differentiation in the Rat Brain Are Dependent on Wnt/β-Catenin Pathway (Molecular Neurobiology, (2015), 52, 3, (1735-1757), 10.1007/s12035-014-8940-1)
(Humana Press Inc., 2019) Shashi Kant Tiwari; Swati Agarwal; Brashket Seth; Anuradha Yadav; Ratan Singh Ray; Vijay Nath Mishra; Rajnish Kumar Chaturvedi
The original version of this article unfortunately contained a mistake. The authors observed inadvertent error in Figure 3A and 6C wish to correct it. The corrected representative images are incorporated below. This correction in no way changes the text of the article, conclusion and figure legend. The authors regret for this error and would like to apologize for any inconvenience caused to the readers. © 2019, Springer Science+Business Media, LLC, part of Springer Nature.
Corrigendum to “PLGA nanoformulation of sparfloxacin enhanced antibacterial activity with photoprotective potential under ambient UV-R exposure” [Int. J. Pharm. 541 (2018) 173–187] (International Journal of Pharmaceutics (2018) 541(1–2) (173–187), (S0378517318301091) (10.1016/j.ijpharm.2018.02.028))
(Elsevier B.V., 2018) Jyoti Singh; Ashish Dwivedi; Lipika Ray; Deepti Chopra; Divya Dubey; Ajeet K. Srivastva; Smita Kumari; Randhir Kumar Yadav; Saroj Kumar Amar; Chandana Haldar; Ratan Singh Ray
The authors regret that mistakes related to image duplication, quality and labeling were found in Fig. 7b Fig. 9 Fig. 10 a. The corrected images are now provided as Figs. 7b, 9c, d and 10a. These mistakes do not change the scientific conclusions of the article in any way. The authors would like to apologise for any inconvenience caused. © 2018 Elsevier B.V.
Corrigendum to “PLGA nanoformulation of sparfloxacin enhanced antibacterial activity with photoprotective potential under ambient UV-R exposure” [Int. J. Pharm. 541 (2018) 173–187](S0378517318301091)(10.1016/j.ijpharm.2018.02.028)
(Elsevier B.V., 2019) Jyoti Singh; Ashish Dwivedi; Lipika Ray; Deepti Chopra; Divya Dubey; Ajeet K. Srivastva; Smita Kumari; Randhir Kumar Yadav; Saroj Kumar Amar; Chandana Haldar; Ratan Singh Ray
The authors regret to inform that there were inadvertent errors in some figures. The corrected images are given below. These corrections are not affecting the results and conclusion of the manuscript. Hence, the text in the original article remains unchanged. The corrected Fig. 8 is as follows: The corrected Fig. 12 is as follows: The authors would like to apologise for any inconvenience caused. © 2019 Elsevier B.V.
Inhibitory Effects of Bisphenol-A on Neural Stem Cells Proliferation and Differentiation in the Rat Brain Are Dependent on Wnt/β-Catenin Pathway
(Humana Press Inc., 2015) Shashi Kant Tiwari; Swati Agarwal; Brashket Seth; Anuradha Yadav; Ratan Singh Ray; Vijay Nath Mishra; Rajnish Kumar Chaturvedi
Neurogenesis, a process of generation of new neurons, occurs throughout the life in the hippocampus and sub-ventricular zone (SVZ). Bisphenol-A (BPA), an endocrine disrupter used as surface coating for packaged food cans, injures the developing and adult brain. However, the effects of BPA on neurogenesis and underlying cellular and molecular mechanism(s) are still unknown. Herein, we studied the effect(s) of prenatal and early postnatal exposure of low dose BPA on Wnt/β-catenin signaling pathway that controls different steps of neurogenesis such as neural stem cell (NSC) proliferation and neuronal differentiation. Pregnant rats were treated with 4, 40, and 400 μg BPA/kg body weight orally daily from gestational day 6 to postnatal day 21. Both in vivo and in vitro studies showed that BPA alters NSC proliferation and differentiation. BPA impaired NSC proliferation (5′-bromo-2′-deoxyuridine (BrdU+) and nestin+ cells) and neuronal differentiation (BrdU/doublecortin+ and BrdU/neuronal nuclei (NeuN+) cells) in the hippocampus and SVZ as compared to control. It significantly altered expression/protein levels of neurogenic genes and the Wnt pathway genes in the hippocampus. BPA reduced cellular β-catenin and p-GSK-3β levels and decreased β-catenin nuclear translocation, and cyclin-D1 and TCF/LEF promoter luciferase activity. Specific activation and blockage of the Wnt pathway suggested involvement of this pathway in BPA-mediated inhibition of neurogenesis. Further, blockage of GSK-3β activity by SB415286 and GSK-3β small interfering RNA (siRNA) attenuated BPA-induced downregulation of neurogenesis. Overall, these results suggest significant inhibitory effects of BPA on NSC proliferation and differentiation in the rat via the Wnt/β-catenin signaling pathway. © 2014, Springer Science+Business Media New York.
Photoaging
(Springer Singapore, 2018) Jyoti Singh; Deepti Chopra; Ashish Dwivedi; Ratan Singh Ray
The incident of photoaging mainly depends upon the intensity of UV-R and the amount of melanin present in the skin. UV-R is known to cause photoaging, photoallergy, and immune suppression to human skin, noted more than a century ago. From last 10 years, several laboratory studies show that UV rays impaired the collagen synthesis, blocked collagen expression, and reduced the elasticity of skin and solar scar formation which is ultimately visible by clinical pattern such atrophy and wrinkle formation. Which further leads to UV-R induced premature aging of the skin. UV radiation alters the ECM by raising the level of matrix metalloproteinases (MMP), decreasing the structural elastin and collagen, directly or indirectly damaging the DNA, and enhancing the cell surface receptors which are present at the surface of keratinocytes and fibroblasts of skin. AP-1 and NF-kB are key signaling molecules which involve in UV-R promoted skin aging. The photoprotective approaches to prevent or treat photocarcinogenesis and photoaging involve natural supplements absorption by orally and topically. Skin accommodates a complex system of endogenous enzymatic and nonenzymatic photoprotective antioxidants. However, their role in the UV-R-induced oxidative damage has not been fully elucidated. Recently, the researchers have elucidated that skin antioxidative defense system is increased in presence of vitamins and nutritive agents and combination of various kinds of antioxidants also produce synergistic results. © Springer Nature Singapore Pte Ltd. 2018.
PLGA nanoformulation of sparfloxacin enhanced antibacterial activity with photoprotective potential under ambient UV-R exposure
(Elsevier B.V., 2018) Jyoti Singh; Ashish Dwivedi; Lipika Ray; Deepti Chopra; Divya Dubey; Ajeet K. Srivastva; Smita Kumari; Randhir Kumar Yadav; Saroj Kumar Amar; Chandana Haldar; Ratan Singh Ray
Sparfloxacin (SPFX) is a broad spectrum antibiotic which inhibits bacterial DNA gyrase enzyme activity. However, photodegradation in the presence of UVA limits its antibacterial activity and induces phototoxicity. Thus, to encounter this problem, we have developed poly d,l-lactic-co-glycolic acid (PLGA) loaded SPFX nanoparticles. Here, we have performed a comparative antibacterial activity of SPFX and its nanoparticles (NPs) through molecular docking and plate sensitivity assay. Under environmental UVA exposure, photoexcited SPFX significantly generates ROS, DNA damage and mitochondrial mediated cell death in comparison to PLGA-SPFX-NPs (nano SPFX) in human skin cell line (HaCaT). In presence of UVA, bulk SPFX induced cell cycle arrest with appearance of sub-G1 peak showing apoptosis while nano SPFX did not show any change. SPFX triggered apoptosis via alteration in membrane integrity of mitochondria and lysosome in comparison to PLGA-SPFX-NPs. Involvement of mitochondrial mediated cell death was confirmed by down-regulation of anti-apoptotic Bcl-2 and procaspase-3 and upregulation of pro-apoptotic Bax, cytochrome-c and caspase-3 proteins expression. Specific caspase inhibitor, Z-VAD-FMK showed involvement of caspase cascade pathway in apoptosis. Our finding suggests that controlled release of SPFX from PLGA-SPFX-NPs can reduce its side effects and enhance its antibacterial activity. Thus, nanotization of fluoroquinolones will be a significant step to reduce the problem of resistance and phototoxicity of this group. © 2018 Elsevier B.V.
RETRACTED: Ambient UV-B exposure reduces the binding of ofloxacin with bacterial DNA gyrase and induces DNA damage mediated Apoptosis (International Journal of Biochemistry and Cell Biology (2016) 73 (111–126), (S1357272516300012), (10.10.1016/j.biocel.2016.01.001))
(Elsevier Ltd, 2019) J. Singh; Ashish Dwivedi; Syed Faiz Mujtaba; Krishna P. Singh; Manish Kumar Pal; Deepti Chopra; Shruti Goyal; Ajeet K. Srivastav; D. Dubey; Shailendra K. Gupta; Chandana Haldar; Ratan Singh Ray
This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief. The study is retracted due to image duplication reasons: The article contains an image that had already appeared in Free Radic Res, 48.3 (2014): 333-346. doi:10.3109/10715762.2013.869324. The images are used in both papers but to conclude something entirely different, and suggested that the images have an entirely different biological meaning and treatment. Duplicating images in this way is ethically not acceptable. © 2019
Synergistic effect of graphene oxide coated nanotised apigenin with paclitaxel (GO-NA/PTX): A ROS dependent mitochondrial mediated apoptosis in ovarian cancer
(Bentham Science Publishers B.V., 2017) Manish Kumar Pal; Shyam Pyari Jaiswar; Ashish Dwivedi; Shruti Goyal; Vinay Nand Dwivedi; Anumesh Kumar Pathak; Vinod Kumar; Pushp Lata Sankhwar; Ratan Singh Ray
Background: Ovarian cancer is most lethal among all gynecologic malignancies. Paclitaxel (PTX) is well used chemotherapeutic regimen for cancer control; however its undesired toxicity has been a matter of concern for clinicians. Here, we used the graphene oxide coated nanotised apigenin (GO-NA) to enhance the efficacy of paclitaxel. Objective: The combined use of paclitaxel (PTX) and nanotised apigenin (NA) may reduce the PTX dose and increase the efficacy. Methods: GO and GO-Apigenin was prepared by modified Hummers method and the nanoparticles were characterized by dynamic light scattering and transmission electron microscopy. SKOV-3 cells were treated by DMSO, Group I (Control)-McCoy's 5A Medium, Group II-Paclitaxel (5nM), Group III- Nanotised Apigenin (GO-NA-10µM), Group IV- Paclitaxel (5nM) + GO-NA (10µM). Cell viability and IC-50 value were determined by MTT assay, synergism by Compusyn software, ROS by DCFH-DA assay, SOD activity by kit and MMP were examined by JC-1 and mitotracker/DAPI staining, cell cycle by flow cytometry, mRNA and protein level by Real Time-PCR and Western blot respectively Results: Results showed that GO-NA-PTX enhanced the anti-proliferative effect in synergistic manner as compare to GO-NA and PTX alone. GO-NA-PTX significantly suppressed the SOD activity, promotes the ROS accumulation, mitochondrial depolarization, DNA integrity and cell cycle arrest collectively accord the apoptosis. Results of immunocytochemistry, RT-PCR and western blot showed up-regulation of caspase-3, Bax, and down-regulation of Bcl-2. Conclusion: The combination of PTX with GO-NA produces synergistic effects in SKOV-3 cells via the modulation of pro and anti-apoptotic gene and may reduce side effects of PTX. © 2017 Bentham Science Publishers.
Synergistic effect of piperine and paclitaxel on cell fate via cyt-c, Bax/Bcl-2-caspase-3 pathway in ovarian adenocarcinomas SKOV-3 cells
(Elsevier B.V., 2016) Manish Kumar Pal; Shyama Pyari Jaiswar; Ajeet Kumar Srivastav; Shruti Goyal; Ashish Dwivedi; Ankit Verma; Jyoti Singh; Anumesh Kumar Pathak; Pushpa Lata Sankhwar; Ratan Singh Ray
Background and aims Ovarian cancer is fourth most common and lethal among all gynecologic malignancies. The chemotherapy usually requires in all stages of ovarian cancer but drugs have several side effects. We hypothesized that use of combination therapy of paclitaxel (PTX) and phytochemical piperine (PIP) may reduce the PTX dose as well as toxicity. The human ovarian adenocarcinomas SKOV3 cell treated with PTX-5 nM and PIP-10 µm after determination of IC50by MTT assay. Reactive oxygen species generation, mitochondrial membrane potential (MMP), DNA damage, cell death pathway markers as release of cyt-c, Bax/Bcl2-caspase-3 and cell cycle arrest were analyzed. The dose dependent treatment of SKOV-3 cells showed IC50and synergism at combination of 5 nM-PTX and 10 µm-PIP in cell viability assay. PTX and PIP increases the accumulation of reactive oxygen species which subsequently leading to increase in JC-1 and fragmented nuclei in mitotracker/DAPI staining. Comet assay showed 4.4-fold increase of tail formation in combined treated cells as compared to control. PTX-PIP arrests the cell cycle in sub-G1 phase. Immunocytochemistry of Bax showed increase in red fluorescence intensity whereas decrease in green fluorescence i.e Bax/Bcl-2 ratio increased. Moreover morphological EB/AO and Hoechst staining confirmed the enhanced apoptosis in combined treatment. Significant upregulation of apoptotic genes, cyt-c (3.4 fold) Bax (2.8 fold), caspase-3 (3.6 fold) whereas no change occurred in Bcl2 mRNA expression and protein expressions. The combination of PTX with PIP produces synergistic effects in SKOV-3 cells via the modulation of pro and anti-apoptotic gene and may compensate the toxicity and side effects of PTX. © 2016
Under ambient UVA exposure, pefloxacin exhibits both immunomodulatory and genotoxic effects via multiple mechanisms
(Elsevier B.V., 2018) Jyoti Singh; Ajeet K. Srivastva; Payal Mandal; Sonam Chandra; Divya Dubey; Ashish Dwivedi; Deepti Chopra; Anurag Tripathi; Ratan Singh Ray
Pefloxacin (PFLX) is an antibiotic, which shows broad spectrum antimicrobial activities. It is an important derivative of fluoroquinolones (FLQs) group. Ultraviolet radiation (200–400 nm) causes major problem for living being which comes at the earth surface naturally through sunlight and increasing regularly due to ozone depletion. PFLX was photodegraded in 5 h and forms photoproduct under UVA exposure. At the non photocytotoxic dose PFLX, shows reduced phagocytosis activity, NO (nitric oxide) production, large vacuole formation and down regulated IL-6, TNF-α and IL-1 in BALB/c macrophages at both genes and proteins levels. At higher doses (photocytotoxic doses), PFLX induced a concentration dependent decrease in cell viability of human keratinocyte cell line (HaCaT) and peritoneal macrophages of BALB/c mice. Our molecular docking suggests that PFLX binds only to the cleaved DNA in the DNA-human TOP2A complex. Topoisomerase assay confirmed that PFLX inhibits human topoisomerase by forming an adduct with DNA. Photosensitized PFLX also caused intracellular ROS mediated DNA damage and formation of micronuclei and cyclobutane pyrimidine dimers (CPDs). Increase intracellular ROS leads to apoptosis which was proved through lysosomal destabilization and reduced mitochondrial membrane potential (MMP). Our present study shows that ambient UVA exposure in the presence of PFLX caused immunomodulatory as well as photogenotoxic effects. Therefore, patients under PFLX drug treatment should avoid sunlight exposure, especially during peak hours for their photosafety. © 2017