Aysun Saricetin

Background/Objectives: Osteoarthritis (OA) is a multifactorial degenerative joint disease characterized by synovial inflammation, oxidative stress, and progressive cartilage degeneration. This study investigated whether intra-articular N-acetylcysteine (NAC) attenuates synovial inflammation and oxidative stress and whether these effects translate into structural cartilage protection. Methods: OA was induced in rats by anterior cruciate ligament transection (ACLT). NAC (5 mg/50 µL) was administered intra-articularly once weekly for three weeks post-ACLT. Inflammatory cytokines (IL-1β, IL-6, TNF-α), oxidative stress markers (iNOS, TAS, TOS, OSI), and cartilage degradation markers (MMP-13, COMP, CTX-II) were quantified in synovial fluid and cartilage homogenates using ELISA. Cartilage integrity was evaluated histologically using the modified Mankin scoring system. Results: Compared with controls, NAC significantly reduced synovial IL-1β, IL-6, TNF-α, MMP-13, and iNOS levels and improved the synovial redox profile by increasing TAS and reducing TOS and OSI (all p < 0.05). In contrast, NAC did not significantly alter cartilage homogenate levels of inflammatory cytokines, oxidative stress indices, or degradation markers (COMP, CTX-II, MMP-13). Histological analysis demonstrated persistent cartilage fissuring, hypocellularity, and proteoglycan loss in both groups (p > 0.05). Conclusions: Intra-articular NAC exerts potent anti-inflammatory and antioxidative effects within the synovial compartment but fails to prevent cartilage degeneration in the ACLT model. These findings indicate a compartment-specific therapeutic profile, suggesting that NAC may function as a symptom-modifying agent in synovitis-dominant OA rather than a structure-modifying therapy. Future studies should focus on optimized delivery systems or combination strategies targeting cartilage and subchondral bone to achieve disease modification.

Background and Objectives: Osteoarthritis (OA) is a degenerative joint disease involving inflammation, oxidative stress, and extracellular matrix (ECM) degradation, leading to cartilage damage and joint dysfunction. This study aimed to evaluate the chondroprotective effects of intra-articular hydrolyzed collagen in a rat model of knee OA using a dual-compartment biochemical and histological approach. Materials and Methods: Twenty male Sprague-Dawley rats underwent ACL transection to induce osteoarthritis and were randomly assigned to receive intra-articular hydrolyzed collagen or saline once weekly for three weeks. At six weeks, knee joints were evaluated histologically using the Mankin score. Synovial fluid and cartilage homogenates were analyzed via enzyme-linked immunosorbent assay (ELISA) for cytokines, cartilage degradation markers, and oxidative stress indicators. Results: The collagen-treated group demonstrated significantly lower Mankin scores. Levels of pro-inflammatory cytokines, interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), as well as cartilage degradation markers, matrix metalloproteinase-13 (MMP-13), C-terminal crosslinked telopeptide of type II collagen (CTX-II), and cartilage oligomeric matrix protein (COMP), were significantly reduced (p < 0.05). Additionally, oxidative stress indicators including inducible nitric oxide synthase (iNOS), total oxidant status (TOS), and oxidative stress index (OSI) were decreased, while total antioxidant status (TAS) was increased in both synovial fluid and cartilage homogenates (p < 0.05). Conclusions: Intra-articular hydrolyzed collagen reduced inflammation, oxidative stress, and extracellular matrix (ECM) degradation, indicating potential chondroprotective effects across both synovial and cartilage compartments.

Folliculogenesis, steroidogenesis, ovulation, and vitellogenesis are regulated by the effect of follicle stimulating hormone (FSH) and luteinizing hormone (LH) in the hypothalamus-pituitary-ovary axis and these hormones act via follicle stimulating hormone receptor (FSHR) and luteinizing hormone receptor (LHR) in the ovary. Poultry ration and food additives are essential in the regulation of reproductive activity. Phytase is a supplement frequently added to laying hen diets to increase phosphorus (P) utilization. The aim of this study was to reveal the effects of a newly isolated microbial phytase together with different concentrations of calcium (Ca2+) and available phosphorus (AP) on ovarian FSHR and LHR expressions. For this purpose, 90 Lohmann LSL-White layers were first divided into three main diet groups (standard Ca2+ and AP, standard Ca2+ and low AP, low Ca2+ and AP) and then into three subgroups (no-phytase, commercial phytase, and microbial phytase). At the end of the experiment, all chickens were slaughtered and ovarian tissues were fixed in formalin. Routine avidin-biotin complex immunohistochemistry was performed using anti-FSHR and anti-LHR primary antibodies. Immunohistochemically, FSHR and LHR were expressed in granulosa/theca cells, oocytes, interstitial cells, and vitellus. While the expression intensity of the receptors increased in the microbial phytase-treated groups, the strongest expression was obtained in the granulosa/theca cells and oocytes in the standard Ca and low AP group. In conclusion, we suggest that the addition of newly isolated microbial phytase to diets of laying hens and feeding standard Ca and low AP may have positive effects on reproductive performance by increasing the FSHR and LHR expression in ovaries.

Purpose Continuous oxygen therapy to compensate for decreased oxygen saturation in the blood is a life-saving treatment used in case lung involvement. Excess oxygen delivery was reported to be a common situation, in which about 50% of the patients showed hyperoxemia and 4% in severe hyperoxemia. In this work, we investigated the effects of hyperoxia on the rat kidneys and whether tadalafil has an effect to reduce this damage. Materials and methods Three groups of 8 male rats each weighing 300–350 g were formed. The groups were divided into the control group, hyperoxia group, and hyperoxia and tadalafil administered group for 10 days. At the end of the 10th day, blood and kidney samples were taken for biochemical analysis (SOD and NO levels) and histopathological examination. Results While our findings showed that SOD levels were significantly different among the control and experimental groups and within the experimental groups, no statistical difference was found in terms of NO levels among the groups (Table 1). While the glomerular and tubular injury was higher in the Hyperoxia group and the Hyperoxia + Tadalafil group than in the control group (p < 0.001), as a result of the rate of severe glomerular and tubular injury in the hyperoxia group, was 62.5% and 43.8% and in the group given tadalafil was 43.8% and 31.3%, respectively (Table 2). Conclusions Exposure to hyperoxia condition causes renal glomerular and tubular damage, and tadalafil does not show a protective effect on this damage according to this study’s dose and exposure time.

Anencephaly is a congenital disease manifesting with the absence of the brain due to the failure of the cranial part of the neural tube to close during the embryonic stage. The disease may be accompanied by other anomalies and usually results in premature death. A stillborn puppy of a 2-year-old female Pomeranian dog is examined in this case. The lack of brain tissue and accompanying abnormal skull formation was noted macroscopically. The eyes were protruding out of their normal position (exophthalmos), and a bifid tongue together with a secondary cleft palate was present. On serial sections stained with Haematoxylin-Eosin, only the medulla spinalis among the central nervous system structures could be inspected microscopically. Immunohistochemistry staining revealed GFAP immunoreactivity in the astrocytic glial cells. NeuN immunoreactivity was detected in the neurons in the medulla spinalis and spinal ganglions. Incomplete retinal layers were observed on the eye sections stained with Haematoxylin-Eosin and NeuN. The case was concluded to be coherent with skull and nervous system congenital malformations rarely observed in dogs. To the best of our knowledge, this represents the first description of a dog with anencephaly, bifid tongue and cleft palate.

This study aimed to investigate the protective effect of tadalafil on reactive oxygen species induced by a hyperoxia model in rats, both in terms of enzymes such as superoxide dismutase (SOD) and nitric oxide (NO), and its pathological effects on the corpus cavernosum. Overall, 24 rats were divided into three groups. The control group (eight rats) was not exposed to any intervention. The second group (eight rats), was exposed to hyperoxia in a hyperoxia cabinet for 8 h a day for 10 days. The third group (eight rats) was exposed to hyperoxia the same as in the second group, tadalafil at a dose of 10 mg/kg was given orally as a dissolved form in water in the amount of 10-12 ml/100 g/day to the rats placed in separate cages having removed from the hyperoxia cabin. SOD levels differ enough to create a difference, but there was no significant difference in terms of NO levels. The SOD level was highest in hyperoxia conditions and lowest in the group given tadalafil. While corpus cavernosum hyperemia was found to be higher statistically in the experimental groups than in the control group, we found that the severity of hyperemia was less in the group given tadalafil. The corpus cavernosum was found to be statistically more dilated in the experimental groups than in the control group. We determined that hyperoxia status increased the level of SOD and this level decreased with tadalafil administration, which would make a statistical difference.