The aim of this study was to evaluate the effects of coenzyme Q10 in the treatment of endometriosis rat models. Twenty seven Sprague Dawley rats were divided into four groups; Control Group (n = 7; Endometriosis group), Reference Group (n = 6; Endometriosis + Buserelin acetate, 20 mg/kg), CoQ10 Group-I (n = 7; Endometriosis + CoQ10, 50 mg/kg) and CoQ10 Group-II (n = 7; Endometriosis + CoQ10, 100 mg/kg). At the end of the experiment, all the rats were sacrificed, and the volume and histoarchitecture of endometrial implants were evaluated. The mast cells were determined by Toluidine blue and collagen fiber density was analysed by Masson’s Trichrome staining. Tumour necrosis factor and vascular endothelial growth factor (VEGF) levels were analysed by enzyme-linked immunosorbent assay in peritoneal fluid and VEGF and matrix metalloproteinase-9 (MMP-9) were evaluated by immunohistochemistry. Terminal deoxynucleotidil transferase-mediated dUTP Nick end labelling (TUNEL) was also used for the detection of apoptotic cells. The CoQ10 treatment significantly decreased the volume of endometriotic implants, VEGF, and MMP-9 immunoreactivity and increased TUNEL-positive cells. The findings of the study suggest that CoQ10 can be used in endometriosis treatment by suppressing the endometriotic implants.

Background: Achilles tendon (AT) midsubstance injuries may heal suboptimally, especially in athletes. Transforming growth factor–beta 3 (TGF-β3) shows promise because of its recently discovered tendinogenic effects. Using poly(lactic-co-glycolic acid)-b-poly(ethylene glycol) (PLGA-b-PEG) nanoparticles (NPs) may enhance the results by a sustained-release effect. Hypothesis: The application of TGF-β3 will enhance AT midsubstance healing, and the NP form will achieve better outcomes. Study Design: Controlled laboratory study. Methods: A total of 80 rats underwent unilateral AT transection and were divided into 4 groups: (1) control (C); (2) empty chitosan film (Ch); (3) chitosan film containing free TGF-β3 (ChT); and (4) chitosan film containing TGF-β3–loaded NPs (ChN). The animals were sacrificed at 3 and 6 weeks. Tendons were evaluated for morphology (length and cross-sectional area [CSA]), biomechanics (maximum load, stress, stiffness, and elastic modulus), histology, immunohistochemical quantification (types I and III collagen [COL1 and COL3]), and gene expression (COL1A1, COL3A1, scleraxis, and tenomodulin). Results: Morphologically, at 3 weeks, ChT (15 ± 2.7 mm) and ChN (15.6 ± 1.6 mm) were shorter than C (17.6 ± 1.8 mm) ( P = .019 and = .004, respectively). At 6 weeks, the mean CSA of ChN (10.4 ± 1.9 mm ² ) was similar to that of intact tendons (6.4 ± 1.1 mm ² ) ( P = .230), while the other groups were larger. Biomechanically, at 3 weeks, ChT (42.8 ± 4.9 N) had a higher maximum load than C (27 ± 9.1 N; P = .004) and Ch (29.2 ± 5.7 N; P = .005). At 6 weeks, ChN (26.9 ± 3.9 MPa) had similar maximum stress when compared with intact tendons (34.1 ± 7.8 MPa) ( P = .121); the other groups were significantly lower. Histologically, at 6 weeks, the mean Movin score of ChN (4.5 ± 1.5) was lower than that of ChT (6.3 ± 1.8). Immunohistochemically, ChN had higher COL3 (1.469 ± 0.514) at 3 weeks and lower COL1 (1.129 ± 0.368) at 6 weeks. COL1A1 gene expression was higher in ChT and ChN at 3 weeks, but COL3A1 gene expression was higher in ChN. Conclusion: The application of TGF-β3 had a positive effect on AT midsubstance healing, and the sustained-release NP form improved the outcomes, more specifically accelerating the remodeling process. Clinical Relevance: This study demonstrated the effectiveness of TGF-β3 on tendon healing on a rat model, which is an important step toward clinical use. The novel method of using PLGA-b-PEG NPs as a drug-delivery system with sustained-release properties had promising results.

Consumption of fructose-rich food and exposure to endocrine disrupting chemicals continue to increase. High fructose consumption is associated with increased incidence of dyslipidemia, hypertension, hyperuricemia and insulin resistance. Bisphenol A (BPA) is an environmental contaminant that exhibits estrogen-like activity; it impairs reproductive organs, sperm production, spermatogenesis and fertility. We investigated the possible ameliorative effects of melatonin on rat epididymis and sperm characteristics following exposure to fructose and BPA. We used 42 adult male Sprague-Dawley rats divided into seven groups. Group 1, control group, was treated with 25 mg/kg sesame oil + 25 mg/kg 0.1% ethanol. Group 2 was treated with 10% aqueous fructose. Group 3 was treated with 25 mg/kg BPA. Group 4 was treated with 10% fructose and 25 mg/kg BPA. Group 5 was treated with 10% fructose and 20 mg/kg melatonin. Group 6 was treated with 25 mg/kg BPA and 20 mg/kg melatonin. Group 7 was treated with 10% fructose, 25 mg/kg BPA and 20 mg/kg melatonin. After 60 days, epididymal tissue was removed and analyzed using histochemistry and immunohistochemistry. Sperm were counted, and sperm motility and viability were investigated. Administration of BPA caused significant damage to both epididymal tissue and sperm quality; melatonin reduced the damage, but did not prevent it completely.

Diabetes mellitus (DM) is a serious and common in the world health problem that leads to different complications. Changes in oxidative stress and antioxidant capacity play an important role in the pathogenesis of DM. The purpose of this study was to investigate ellagic acid (EA) treatment in diabetes induced testicular damage. In our study, 24 male Sprague Dawley rats were divided into four groups. Group 1: Control (n = 6), Group 2: EA (n = 6), Group 3: Diabet (n = 6), Group 4: Diabet + EA (n = 6). Diabetes was induced by intraperitoneal injection of streptozocin (STZ) (55 mg/kg) to group 3 and 4. EA was given 100 mg/kg/day group 2 and 4 for 35 days by oral gavage. We used that Hematoxylen-Eosin (H&E) and Johnsen’s scoring to determine histological change. The terminal-deoxynucleoitidyl-transferase mediated nick end-labeling assay (TUNEL) was used for apoptosis. Oxidative stress markers were determined by qRT-PCR and immunexpression of Nrf2 was evaluated in testicular tissue. In conclusion, EA administration on the diabetes model has changed the histopathological features, apopotosis and oxidative stress marker genes in the testis and may have an effect on the reduction of diabetes induced testicular damage.