http://nopr.niscpr.res.in/handle/123456789/67841 2026-10-12T12:33:53Z 2026-10-12T12:33:53Z I Khan, Tahir Kumar S, Aakash S Patel, Snehal N Shah, Jigar http://nopr.niscpr.res.in/handle/123456789/67869 2026-06-02T05:10:49Z 2026-05-01T00:00:00Z

Title: Unraveling diabetic retinopathy: mechanisms, novel targets, and the need for continued innovation Authors: I Khan, Tahir; Kumar S, Aakash; S Patel, Snehal; N Shah, Jigar Abstract: Diabetes is a chronic disease and it is a group of metabolic disorders characterized by elevated levels of blood glucose, which results in microvascular complications. The most frequent consequence of microvascular complications is diabetic retinopathy. The pathophysiology of diabetic retinopathy is multifactorial and is associated with several interdependent mechanisms, involving the interplay between hyperglycemia, hyperlipidemia, hypoxia, reactive oxygen species (ROS), inflammation, and neovascularization. Diabetic retinopathy is largely asymptomatic and, by the time-impaired vision is experienced, the pathology may be significantly advanced from non-proliferative to more severely proliferative, in which the abnormal growth of new vessels occurs. Treatment options for diabetic retinopathy include laser treatment, vitrectomy, and a single or a combination of medications. Artificial intelligence tools and Gene editing are futuristic ways of approaching retinopathy treatment. These treatments and techniques either need the use of anesthesia or long-term hospitalization, or to be injected repeatedly and can cause mild discomfort and systemic side effects. The anti-vascular endothelial growth factor alone or with steroids showed some therapeutic benefits. The treatment for diabetic retinopathy is still challenging. Continuous research and development in this field are crucial to improve outcomes for individuals affected by retinopathy, reducing the burden of this vision-threatening complication of diabetes. Page(s): 361-373

2026-05-01T00:00:00Z BERK AHU, Emre PANDIR, Dilek UNSAL BARAK, Mehmet http://nopr.niscpr.res.in/handle/123456789/67865 2026-06-02T05:05:41Z 2026-05-01T00:00:00Z

Title: Different cellular responses to Artemisinin in cancer and normal cells: evaluation of cytotoxic, genotoxic and antioxidant effects with in silico molecular docking Authors: BERK AHU, Emre; PANDIR, Dilek; UNSAL BARAK, Mehmet Abstract: Artemisinin is a natural compound that exhibits cytotoxic effects, particularly on cancer cells. This study investigated the effects of Artemisinin on the cytotoxic, genotoxic, and antioxidant enzyme activities of the human breast cancer cell line (MDA-MB-231) and the normal fibroblast cell line (L929) with molecular docking. Cells were treated with Artemisinin at concentrations of 12.5 μM, 25 μM, and 50 μM. Cell viability was assessed using the MTT assay, DNA damage using the comet assay, and antioxidant enzyme activities (SOD, CAT, GPx) using the ELISA method. MTT analysis revealed a dosedependent decrease in viability in MDA-MB-231 cells, with an LD50 value determined to be 25 μM. In L929 cells, viability was preserved up to 25 μM, but a decrease was observed at 50 μM. Comet assay results showed that DNA damage increased in a dose-dependent manner in MDA-MB-231 cells, while in L929 cells, significant damage occurred only at 50 μM. Antioxidant enzyme analyses revealed significant decreases in SOD, CAT, and GPx activities in MDA-MB-231 cells, while no changes were observed in L929 cells at 25 μM, and enzyme activities decreased at 50 μM. Artemisinin produces cytotoxic and genotoxic effects in cancer cells with showed molecular docking parameter, while exhibiting lower toxicity at low concentrations in normal cells. Page(s): 374-382

2026-05-01T00:00:00Z Demirtaş, Selim Polat Sarı, Silva Aytaç Türkan, Fulya Ceyda Sözüer, Emine Seker, Ugur Büyükkılıç Altınbaşak, Betül Sahika Gokdemir, Gul http://nopr.niscpr.res.in/handle/123456789/67863 2026-06-02T04:57:18Z 2026-05-01T00:00:00Z

Title: Protective effects of gilaburu (Viburnum opulus L.) fruit extract on testicular damage in streptozotocin induced diabetic rats Authors: Demirtaş, Selim; Polat Sarı, Silva; Aytaç Türkan, Fulya; Ceyda Sözüer, Emine; Seker, Ugur; Büyükkılıç Altınbaşak, Betül; Sahika Gokdemir, Gul Abstract: Diabetes mellitus (DM) causes the impairment of male reproductive functions by inducing oxidative stress and apoptosis in testicular tissues. Despite various therapeutic approaches, the need for effective strategies to reduce diabetes-related testicular damage remains a significant issue. In this study, the potential protective effects of Gilaburu fruit extract, known for its potent antioxidant and anti-inflammatory properties, were investigated against streptozotocin (STZ)-induced testicular damage. Subjects were divided into control, diabetes (STZ, 50 mg/kg), and treatment (DM+Glb; 200 mg/kg Gilaburu) groups. While serum testosterone levels were measured, malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase 1 (GPx1) levels, along with histopathological parameters and immunohistochemical markers (Bax, Bcl-2, PCNA, and Sirt6), were evaluated in testicular tissues. In the diabetes group, testosterone, SOD, and GPx1 levels significantly decreased, while MDA levels and the Bax/Bcl-2 ratio increased. These biochemical changes were accompanied by a narrowing of seminiferous tubule diameters and a decrease in PCNA and Sirt6 expressions. Gilaburu treatment significantly improved these impairments by reducing oxidative stress, inhibiting apoptosis, and increasing cellular proliferation and Sirt6 levels. In conclusion, Gilaburu extract may demonstrate potential as a supportive phytotherapeutic agent against diabetes-related testicular damage by regulating the oxidative stress-apoptosis-proliferation axis. Page(s): 383-393

2026-05-01T00:00:00Z Jinxing, Guo Jiahang, Hu Dan, Fu http://nopr.niscpr.res.in/handle/123456789/67861 2026-06-02T04:50:08Z 2026-05-01T00:00:00Z

Title: Effective method for studying β5 subunit activity of immunoproteasome in vitro Authors: Jinxing, Guo; Jiahang, Hu; Dan, Fu Abstract: The immunoproteasome and its dysfunction are implicated in multiple diseases. In multiple myeloma, immunoproteasomes promote cancer cell survival, making them an important therapeutic target for antagonist development. Here, we present a straightforward method for detecting β5i (the β5 subunit of the immunoproteasome) cellular activity in vitro. This cell-based approach utilizes a specific β5i substrate (Ac-Ala-Asn-Trp-AMC), which is cleaved by immunoproteasomes and releases a fluorescent signal with an emission peak at 460 nm. After multiple optimizations, we found that adding an equal volume of substrate solution to 30 μL cell lysate, incubating for 10 minutes at 37°C, and measuring fluorescence at 460 nm yielded IC₅₀ values for ONX-0914 (a selective inhibitor of low-molecular mass polypeptide-7) and bortezomib that are consistent with published data, with repeatable and stable results across different cell lines. Additionally, comparison with the β5c commercial kit (Promega, G8661), which is compatible with the β5c substrate, demonstrated excellent sensitivity and accuracy. In summary, this protocol facilitates the screening and determination of subunit specificity for novel immunoproteasome inhibitors. Page(s): 394-399

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