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Al Kury LT, Zeb A, Abidin ZU, et al. Drug Des Devel Ther. 2019;13:2715–2727. In the published article, there was an error in Figure 4B on page 2723. The image for Ethanol+celecoxib+mela (Piriform-PIR) was used mistakenly leading to a duplication with the Control (Piriform-PIR) images. A new image for Ethanol+celecoxib+mela (Piriform-PIR) was found from the original data and used as a replacement. The authors apologize for this error and state that this does not change the quality and scientific conclusions of the article. The correct Figure 4 is as follows. Figure 4 Effect of melatonin and celecoxib on neuronal cell death.Notes: (A) Regions of interest analyzed; (B) H&E staining showing the extent of surviving neurons in the cortex and hippocampus. Bar 50 μm, magnification 20×, n=5/group. Surviving neurons were marked by cytoplasmic swelling, scalloped neurons with intense cytoplasmic eosinophilia, and nuclear basophilia. These changes resulted from neuronal necrosis. Some cells had a shrunken appearance, along with pyknotic nuclei. Intensive neuropil vacuolation can be seen in the ethanol-only group. *Significant difference relative to control; #Significant difference relative to ethanol group; θSignificant difference relative to ethanol + melatonin. Data presented as means ± SEM. Data analyzed by one-way ANOVA followed by post hoc Bonferroni multiple comparison using GraphPad Prism 5 software. ***P

Komal Naeem,1,2,* Lina Tariq Al Kury,3 Faiza Nasar,1,* Abdullah Alattar,4 Reem Alshaman,4 Fawad Ali Shah,1 Arif-ullah Khan,1 Shupeng Li2 1Department of Pharmacology, Faculty of Pharmaceutical Sciences, Riphah International University, Islamabad, 747424, Pakistan; 2State Key Laboratory of Oncogenomics, School of Chemical Biology and Biotechnology, Shenzhen Graduate School, Peking University, Shenzhen, 518000, People’s Republic of China; 3College of Natural and Health Sciences, Zayed University, Abu Dhabi, 49153, United Arab Emirates; 4Department of Pharmacology and Toxicology, Faculty of Pharmacy, University of Tabuk, Tabuk, 71421, Saudi Arabia*These authors contributed equally to this workCorrespondence: Fawad Ali ShahDepartment of Pharmacology, Faculty of Pharmaceutical Sciences, Riphah International University, 7th Avenue, Sector G-7/4, Islamabad, 747424, PakistanTel +92-51-2891835-38Fax +92-51-2891471Email fawad.shah@riphah.edu.pkShupeng LiState Key Laboratory of Oncogenomics, School of Chemical Biology and Biotechnology, Shenzhen Graduate School, Peking University, Shenzhen, 518000, People’s Republic of ChinaEmail lisp@pku.edu.cnPurpose: Major depressive disorder (MDD) is a debilitating human health condition characterized by mood swings and is associated with a high probability of suicide attempts. Several studies have reported a role of neuroinflammation in MMD, yet the efficacy of natural drug substances on neuroinflammation-associated depression has not been well-investigated. The present study examined the neuroprotective effects of carvacrol on lipopolysaccharide (LPS)-induced neuroinflammation, depression, and anxiety-like behavior.Methods: Male Sprague Dawley rats were divided into two experimental cohorts to determine the effects and the effective dose of carvacrol (whether 20 mg/kg or 50 mg/kg), and further demonstrate the mechanism of action of nuclear factor E2-related factor (Nrf2) in depression.Results: We found marked neuronal alterations in the cortex and hippocampus of LPS-intoxicated animals that were associated with higher inflammatory cytokine expression such as cyclooxygenase (COX2), tumor necrosis factor-alpha (TNF-α), and c-Jun N-terminal kinase (p-JNK). These detrimental effects exacerbated oxidative stress, as documented by a compromised antioxidant system due to high lipid peroxidase (LPO). Carvacrol (20 mg/kg) significantly reverted these changes by positively modulating the antioxidant gene Nrf2, a master regulator of the downstream antioxidant pathway. To further investigate the role of Nrf2, an inhibitor of Nrf2 called all-trans retinoic acid (ATRA) was used, which further exacerbated LPS toxicity with a higher oxidative and inflammatory cytokine level. To further support our notion, we performed virtual docking of carvacrol with the Nrf2-Keap1 target and the resultant drug-protein interactions validated the in vivo findings.Conclusion: Collectively, our findings suggest that carvacrol (20 mg/kg) could activate the endogenous master antioxidant Nrf2, which further regulates the expression of downstream antioxidants, eventually ameliorating LPS-induced neuroinflammation and neurodegeneration.Keywords: depression, neuroinflammation, Nrf2 pathway, lipopolysaccharide, carvacrol, neurodegeneration

Zulkifal Malik,1,2 Muzaffar Abbas,2 Lina Tariq Al Kury,3 Fawad Ali Shah,1 Mahboob Alam,2 Arif-ullah Khan,1 Humaira Nadeem,1 Saad Alghamdi,4 Muhammad Umar Khayam Sahibzada,5 Shupeng Li6 1Riphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad, Pakistan; 2Faculty of Pharmacy, Capital University of Science and Technology, Islamabad, Pakistan; 3College of Natural and Health Sciences, Zayed University, Abu Dhabi, United Arab Emirates; 4Laboratory Medicine Department, Faculty of Applied Medical Sciences, Umm Al-Qura University, Mecca, Saudi Arabia; 5Department of Pharmacy, Sarhad University of Science and Information Technology, Peshawar, KPK, Pakistan; 6State Key Laboratory of Oncogenomics, School of Chemical Biology and Biotechnology, Shenzhen Graduate School, Peking University, Shenzhen, People’s Republic of ChinaCorrespondence: Muzaffar AbbasFaculty of Pharmacy, Capital University of Science and Technology, Islamabad Expressway, Kahuta Road, Zone-V, Islamabad, PakistanTel +92-51-111555666Fax +92-51-4486705Email Muzaffar.abbas@cust.edu.pkShupeng LiState Key Laboratory of Oncogenomics, School of Chemical Biology and Biotechnology, Shenzhen Graduate School, Shenzhen, 518055, People’s Republic of ChinaEmail lisp@pku.edu.cnBackground: Peripheral inflammation leads to the development of persistent thermal hyperalgesia and mechanical allodynia associated with increased expression of interleukin-1β (IL-1β) in the spinal cord. The aim of the present study was to investigate the effects of thiazolidine derivatives, 1b ([2-(2-hydroxyphenyl)-1,3-thiazolidin-4-yl](morpholin-4-yl)methanone) and 1d (2-hydroxy-4-{[2-(2-hydroxyphenyl)-1,3-thiazolidine-4-carbonyl]amino}benzoic acid), on thermal hyperalgesia, mechanical allodynia and on IL-1β expression during carrageenan-induced inflammation in the spinal cord in mice. Inflammatory pain was induced by injecting 1% carrageenan into the right hind paw of the mice.Methods: The animals were administered thiazolidine derivatives, 1b and 1d (1 mg/kg, 3 mg/kg, or 10 mg/kg), intraperitoneally 30 minutes before carrageenan administration. The animals’ behavior was evaluated by measuring thermal hyperalgesia, mechanical allodynia, and motor coordination. The IL-1β expression was measured by enzyme-linked immunosorbent assay. Acute and sub-acute toxicity studies were conducted to evaluate the toxicity profile of compounds.Results: Treatment with the thiazolidine derivative, 1b and 1d, attenuated carrageenan-induced thermal hyperalgesia and mechanical allodynia at doses of 1 mg/kg, 3 mg/kg, and 10 mg/kg. No motor coordination deficits were observed in animals. The compounds also reduced IL-1β expression in the spinal cord of mice. Acute and sub-acute toxicity studies revealed that both compounds were safe.Conclusion: The compounds exhibit promising activity against inflammatory pain due to their ability to produce anti-hyperalgesic and anti-allodynic effects and to inhibit IL-1β expression in the spinal cord.Keywords: inflammatory pain, IL-1β, thiazolidine derivatives, mechanical allodynia, thermal hyperalgesia

Naeem K, Tariq Al Kury L, Nasar F, et al. J Inflamm Res. 2021;14:1313–1329. At the authors request, the Editor and Publisher of Journal of Inflammation Research wish to retract the published article. The authors became aware of suspected duplicated images in Figures 4 and 5 and requested for the article to be retracted. Specifically, Figure 4B, Bcl-2, Hippocampus, FLX+LPS appears to have been duplicated with the same image for Figure 4C, Caspase-3, Hippocampus, CAR 20+LPS. Figure 5D, TNF-α, Cortex, LPS appears to have been duplicated with the same image for Figure 5D, TNF-α, Cortex, CAR 20+ATRA+LPS. Figure 5D, TNF-α, Cortex, ATRA+LPS appears to have been duplicated with the same image for Figure 5E, p-NFκB, Cortex, ATRA+LPS (which has been flipped). The Editor agreed with the authors retraction request and the authors were notified of this. Our decision-making was informed by our policy on publishing ethics and integrity and the COPE guidelines on retraction. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”.

Lina T Al Kury,1 Alam Zeb,2 Zain Ul Abidin,2 Nadeem Irshad,3 Imran Malik,2 Arooj Mohsin Alvi,2 Atif Ali Khan Khalil,4 Sareer Ahmad,4 Muhammad Faheem,2 Arif-Ullah Khan,2 Fawad Ali Shah,2 Shupeng Li51College of Natural and Health Sciences, Zayed University, Abu Dhabi, United Arab Emirates; 2Riphah Institute of Pharmaceutical Sciences, Riphah International University, Islamabad, Pakistan; 3Department of Pharmacy, Quaid-I-Azam University, Islamabad, Pakistan; 4Rehman Medical Institute, Peshawar, Pakistan; 5State Key Laboratory of Oncogenomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen 518055, People’s Republic of ChinaPurpose: Melatonin and celecoxib are antioxidants and anti-inflammatory agents that exert protective effects in different experimental models. In this study, the neuroprotective effects of melatonin and celecoxib were demonstrated against ethanol-induced neuronal injury by in silico, morphological, and biochemical approaches.Methods: For the in silico study, 3-D structures were constructed and docking analysis performed. For in vivo studies, rats were treated with ethanol, melatonin, and celecoxib. Brain samples were collected for biochemical and morphological analysis.Results: Homology modeling was performed to build 3-D structures for IL1β), TNFα, TLR4, and inducible nitric oxide synthase. Structural refinement was achieved via molecular dynamic simulation and processed for docking and postdocking analysis. Further in vivo experiments showed that ethanol induced marked neuronal injury characterized by downregulated glutathione, glutathione S-transferase, and upregulated inducible nitric oxide synthase. Additionally, ethanol increased the expression of TNFα and IL1β. Finally, neuronal apoptosis was demonstrated in ethanol-intoxicated animals using caspase 3 and activated JNK staining. On the other hand, melatonin and celecoxib treatment ameliorated the biochemical and immunohistochemical alterations induced by ethanol.Conclusion: These results demonstrated that ethanol induced neurodegeneration by activating inflammatory and apoptotic proteins in rat brain, while melatonin and celecoxib may protect rat brain by downregulating inflammatory and apoptotic markers.Keywords: simulation, docking, cortex, hippocampus, ethanol, neurodegeneration

Shakir Khan,1 Fahad Alam,2 Ameer Azam,2 Asad U Khan11Interdisciplinary Biotechnology Unit, 2Center of Excellence in Material Science (Nanomaterials), Aligarh Muslim University, Aligarh, IndiaAbstract: This article explores the novel gold nanoparticle–enhanced photodynamic therapy of methylene blue against recalcitrant pathogenic Candida albicans biofilm. Physiochemical (X-ray diffraction, ultraviolet-visible absorption, photon cross-correlation, FTIR, and fluorescence spectroscopy) and electron microscopy techniques were used to characterize gold nanoparticles as well as gold nanoparticle–methylene blue conjugate. A 38.2-J/cm2 energy density of 660-nm diode laser was applied for activation of gold nanoparticle–methylene blue conjugate and methylene blue against C. albicans biofilm and cells. Antibiofilm assays, confocal laser scanning, and electron microscopy were used to investigate the effects of the conjugate. Physical characteristics of the gold nanoparticles (21 ± 2.5 nm and 0.2 mg/mL) and methylene blue (20 µg/mL) conjugation were confirmed by physicochemical and electron microscopy techniques. Antibiofilm assays and microscopic studies showed significant reduction of biofilm and adverse effect against Candida cells in the presence of conjugate. Fluorescence spectroscopic study confirmed type I photo toxicity against biofilm. Gold nanoparticle conjugate–mediated photodynamic therapy may be used against nosocomially acquired refractory Candida albicans biofilm.Keywords: Candida biofilm, gold nanoparticle–methylene blue conjugate, photodynamic therapy

Asad U KhanMedical Microbiology and Molecular Biology Laboratory, Interdisciplinary Biotechnology Unit, Aligarh Muslim University, Aligarh, IndiaThis is with reference to an article published recently in your journal regarding the antibiotic activity of chitosan-coated silver nanoparticles.1 This is an inspiring move towards control of infection caused by multidrug-resistant bacteria which has become a serious problem for clinicians and physicians worldwide.2 At the moment, carbapenems are being used as the drugs of choice to combat infections. However, the emergence of carbapenem resistance has changed current remedial approaches in the management of serious infections. One of the latest enzymes, NDM-1 (New Delhi metallo-β-lactamase-1), first identified in a Swedish patient of Indian origin in 2008,3 has been key in the development of resistance to almost all antibiotics. Infection caused by NDM-1 producers is widespread on the Indian subcontinent,4 and is now emerging in the US and other countries throughout the world.5View original paper by Jena and colleagues.

Asad U KhanMedical Microbiology and Molecular Biology Laboratory, Interdisciplinary Biotechnology Unit, Aligarh Muslim University, Aligarh, IndiaConcerning the recent article published in your journal on antibiofilm surface functionalization of catheters.1 This is an admirable approach to inhibit biofilm formation on the surfaces of various implants. Currently, a number of biomedical devices and implants are commonly used in hospitals and clinics. Over the past few decades, a number of knee and hip implants have been introduced to save lives and restore quality of life. Moreover, a significant increase in the use of stents, heart valves, vascular grafts, catheters, and other implantable devices are being introduced worldwide. However, regrettably, these surfaces are prone to microbial infections and hence device-related infections have become a major source of infection which may ultimately lead to a high mortality rate in the hospital setting.2View original paper by Lellouche and colleagues.