Sürdürülebilir Kalkınma Amaçları

• 3

Yazarlar

• Erten, Fusun(2)
• Sahin, Kazim(2)
• Aksu, Emrah Hicazi(1)
• Benzer, Fulya(1)
• Bilgic, Ahmet Alp(1)
• Caglayan, Ahmet Burak(1)
• Dhavan, Nanasaheb(1)
• Dogan, Tuba(1)
• Dortbudak, Muhammet Bahaeddin(1)
• Genc, Aydin(1)
• Gunal, Mehmet Yalcin(1)
• Ileriturk, Mustafa(1)
• Kandemir, Fatih Mehmet(1)
• Kilic, Ertugrul(1)
• Kursun, Oznur Ece Durmaz(1)
• Lal, Mohan(1)
• Morde, Abhijeet(1)
• Orhan, Cemal(1)
• Ozercan, Ibrahim Hanifi(1)
• Padigaru, Muralidhara(1)
• Sahin, Emre(1)
• Sahin, Nurhan(1)
• Sakul, Ayse Arzu(1)
• Yildirim, Serkan(1)

• MakaleAçık Erişim2023Scopus SJRQ1/r/munzur/1979
  Lutein/Zeaxanthin Isomers and Quercetagetin Combination Safeguards the Retina from Photo-Oxidative Damage by Modulating Neuroplasticity Markers and the Nrf2 Pathway

  Sahin, Emre; Orhan, Cemal; Sahin, Nurhan; Padigaru, Muralidhara; Morde, Abhijeet; Lal, Mohan; Dhavan, Nanasaheb; Erten, Fusun; Bilgic, Ahmet Alp; Ozercan, Ibrahim Hanifi

  Exposure to light-emitting diode (LED) light is a primary cause of retinal damage, resulting in vision loss. Several plant-derived substances, such as lutein and quercetagetin (QCG), show promise in supporting eye health. In this study, the impact of lutein/zeaxanthin (L/Z, Lutemax 2020) and QCG were evaluated individually and together in a rat model of LED-induced retinal damage. A total of 63 Wistar rats were allocated into nine groups (n = 7). For 28 days, the rats received L/Z (10 or 20 mg/kg BW), quercetin (QC, 20 mg/kg BW), QCG (10 or 20 mg/kg BW), or a mixture of different lutein and QCG dosages, after which they were exposed to LED light for 48 h. LED exposure led to a spike in serum malondialdehyde (MDA) and inflammatory cytokines, as well as an increase in retinal NF-κB, ICAM, GFAP, and MCP-1 levels (p < 0.0001 for all). It also reduced serum antioxidant enzyme activities and retinal Nrf2, HO-1, GAP43, NCAM, and outer nuclear layer (ONL) thickness (p < 0.0001 for all). However, administering L/Z and QCG, particularly a 1:1 combination of L/Z and QCG at 20 mg/kg, effectively reversed these changes. The treatment suppressed NF-κB, ICAM, GFAP, and MCP-1 while enhancing Nrf2, HO-1, GAP43, and NCAM and preventing ONL thickness reduction in LED-induced retinal damage rats. In conclusion, while LED light exposure caused retinal damage, treatment with L/Z, QC, and QCG, particularly a combined L/Z and QCG regimen, exhibited protective effects on the retina. This is possibly due to the modulation of neuroplasticity markers and nuclear transcription factors in the rats’ retinal cells.

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  AtıfScopus22·OpenAlex22

  İncele
• MakaleAçık Erişim2021Scopus SJRQ2/r/munzur/2931
  Protective Effect of Lutein/Zeaxanthin Isomers in Traumatic Brain Injury in Mice

  Gunal, Mehmet Yalcin; Sakul, Ayse Arzu; Caglayan, Ahmet Burak; Erten, Fusun; Kursun, Oznur Ece Durmaz; Kilic, Ertugrul; Sahin, Kazim

  Previous studies revealed that oxidative stress and inflammation are the main contributors to secondary injury after traumatic brain injury (TBI). In an earlier study, we reported that lutein/zeaxanthin isomers (L/Zi) exert antioxidative and anti-inflammatory effects by activating the nuclear factor-kappa B (NF-κB) and nuclear factor-erythroid 2-related factor 2 (Nrf2) pathways. However, its precise role and underlying mechanisms were largely unknown after TBI. This study was conducted to investigate the potential mechanism of L/Zi isomers in a TBI model induced by a cold injury model in mice. To investigate the effects of L/Zi, male C57BL/6j mice-induced brain injury using the cold trauma model was allocated into two groups (n = 7): (i) TBI + vehicle group and (ii) TBI + L/Zi group (20 mg/kg BW). Brain samples were collected 24 h later for analyses. L/Zi given immediately after the injury decreased infarct volume and blood–brain barrier (BBB) permeability; L/Zi treatment also significantly reduced proinflammatory cytokines, including interleukin1 beta (IL-1β), interleukin 6 (IL-6), and NF-κB levels and increased growth-associated protein 43 (GAP-43), neural cell adhesion molecule (NCAM), brain-derived neurotrophic factor (BDNF), and Nrf2 levels compared with vehicle control. These data suggest that L/Zi improves mitochondrial function in TBI models, possibly decreasing inflammation and activating the Nrf2 pathway.

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  AtıfScopus39·OpenAlex40

  İncele
• MakaleYalnız künye2021Scopus SJRQ2/r/munzur/2917
  Chrysin protects against testicular toxicity caused by lead acetate in rats with its antioxidant, anti-inflammatory, and antiapoptotic properties

  Ileriturk, Mustafa; Benzer, Fulya; Aksu, Emrah Hicazi; Yildirim, Serkan; Kandemir, Fatih Mehmet; Dogan, Tuba; Dortbudak, Muhammet Bahaeddin; Genc, Aydin

  In the present study, the protective effects of chrysin (CHR) against testicular damage caused by lead acetate (PbAc) were examined. In this way, 30 min after rats were given 25 and 50 mg/kg/b.w CHR orally for seven consecutive days, 30 mg/kg/b.w PbAc was administered orally. In biochemical analysis of testicular tissue, it was found that PbAc-reduced antioxidant parameters [glutathione peroxidase (GPx), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT)], while it increased lipid peroxidation, inflammatory markers [nuclear factor kappa-B (NF-κB), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE-2), and inducible nitric oxide synthase (iNOS)], and 8-hydroxy-2′-deoxyguanosine (8-OHdG). In the immunohistochemical examination, it was determined that PbAc increased the expression of tumor necrosis factor-α (TNF-α) and caspase-3. Accordingly, PbAc was found to cause a decrease in sperm motility and an increase in the percentage of dead sperm. However, it has been observed that CHR relieves oxidative stress due to its antioxidant properties, thus protecting against inflammation and apoptosis. It also allowed the CHR sperm parameters to return to control group levels. The results revealed that CHR could be a natural substance to be used in Pb-induced testicular toxicity. Practical applications: Lead (Pb) is an important environmental contaminant heavy metal. Pb is believed to reduce fertility in men. Oxidative stress plays a significant role in the damage caused by Pb to testicular tissue. CHR is an antioxidant substance that occurs naturally in various plants and has various pharmacological properties. In the present study, it was investigated whether CHR has a protective effect against testicular toxicity induced by PbAc. The results revealed that in rats, CHR protects the testicular tissue from PbAc toxicity by showing antioxidant, anti-inflammatory and anti-apoptotic effects, thus bringing sperm parameters closer to normal.

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  AtıfScopus76·WoS71·OpenAlex81

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