Dexmedetomidine protects the uterus against ischemia-reperfusion injury in rats.

OBJECTIVE: This study aimed to analyze the histopathological and biochemical effects of dexmedetomidine on the rat uteri exposed to experimental ischemia-reperfusion injury. MATERIALS AND METHODS: Twenty-four female rats were randomly divided into three groups. Group 1 was defined as the control group. An experimental uterine ischemia-reperfusion model was created in Group 2. Group 3 was assigned as the treatment group. Similar uterine ischemia-reperfusion models were created for the rats in Group 3, and then, unlike the other groups, 100 µg/kg of dexmedetomidine was administered intraperitoneally immediately after the onset of reperfusion. In blood biochemical analysis, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities and malondialdehyde (MDA), interleukin 1beta (IL-1ß), interleukin 6 (IL-6) and tumor necrosis factor-alpha (TNF-α) levels were measured. In the histopathological analyses, endometrial epithelial glandular changes (leukocytosis, cell degeneration) and endometrial stromal changes (congestion, edema) were analyzed using the tissue damage scoring system. RESULTS: It was observed that IL-1ß, IL-6, and TNF-α levels were significantly suppressed in Group 3 compared to Group 2 (p=0.001, p<0.001 and p=0.001, respectively). MDA level was noted as the highest in Group 2. The MDA value in Group 3 was measured at 5.37±0.82, which was significantly decreased compared to Group 2 (p<0.001). An increase in antioxidant enzyme activities (SOD and GSH-PX) was observed in Group 3 compared to Group 2 (p=0.001 and p=0.006, respectively). In our histopathological analysis, a significant improvement in endometrial epithelial glandular and endometrial stromal changes was revealed in Group 3 compared to Group 2 (p<0.001). CONCLUSIONS: In our study, it has been documented that dexmedetomidine protects the uterine tissue against ischemia-reperfusion injury.

Detection of nuclear receptors in gingival samples of diabetic and nondiabetic periodontitis patients.

BACKGROUND: Diabetes and periodontitis are two chronic inflammatory diseases sharing specific etiopathogenetic mechanisms, and both cause severe inflammation and destruction. AIMS: The present study aimed to determine the receptor expressions of peroxisome proliferative-activated receptor (PPAR)-γ, retinoid X receptor (RXR)-α, vitamin D receptor (VDR), and nuclear factor kappa B (NF-κB) expressions in healthy gingiva and diseased gingival samples with or without diabetes. METHODS: Forty-five participants as (1) healthy controls (C), (2) periodontitis group (P), and (3) diabetes and periodontitis group (DP) were enrolled. Plaque index (PI), gingival index (GI), probing depth (PD), clinical attachment levels (CAL), and bleeding on probing (BOP) were recorded in all participants. Two gingival biopsies from each participant were obtained, and one underwent histological tissue processing while the other underwent qRT-PCR analysis of nuclear receptors. Inflammatory and fibroblast cell counts, PPAR-γ, RXR-α, VDR, and NF-κB were evaluated. RESULTS: Fibroblast cells were lowest in the DP group and highest in the healthy group. PPAR-γ, VDR, RXR, and NF-κB expressions were higher in the healthy controls in the qRT-PCR analysis and similar in the other groups. Immunohistochemistry analysis also showed similar results. CONCLUSION: qRT-PCR results concluded that healthy gingival samples had higher PPAR-γ, RXR, VDR, and NF-κB expressions, and immunohistochemistry findings supported the results. In addition, healthy gingiva contained higher fibroblast cells and lower inflammatory cells.

PPAR-γ, RXR, VDR, and COX-2 Expressions in gingival tissue samples of healthy individuals, periodontitis and peri-implantitis patients.

OBJECTIVE: Periodontitis and peri-implantitis are irreversible destructive diseases of periodontal and peri-implant tissues. This study aimed to determine the receptor expressions of peroxisome proliferative-activated receptor (PPAR)-γ, retinoid X receptor (RXR)-α, vitamin D receptor (VDR), and cyclooxygenase (COX)-2 in diseased tissues around teeth and dental implants. SUBJECTS AND METHODS: The study consisted of three groups: group 1, healthy group (C, n = 15); group 2, periodontitis patients with stage 3 grade B (P, n = 15); and group 3, peri-implantitis patients (PI, n = 15). Periodontal clinical parameters such as the plaque index (PI), gingival index (GI), and probing pocket depths (PPD) were recorded. Gingival and peri-implant mucosal biopsies were obtained from all participants and biopsy samples underwent histological tissue processing. Hematoxylin-eosin (H & E) and immunohistochemistry staining were performed. Total inflammatory cell counts and fibroblast cell density were evaluated on H and E-stained slides, while PPAR-γ, RXR-α, VDR, and COX-2 were evaluated through immunohistochemistry. RESULTS: The age of participants were similar, while PI, GI, and PPD values were higher in periodontitis and peri-implantitis groups compared with healthy group. Inflammatory cell infiltration was higher in periodontitis and peri-implantitis compared with healthy group, while fibroblast cell density exhibited a reverse pattern. PPAR-γ and also COX-2 expressions were lower in the healthy group and higher in periodontitis and peri-implantitis groups. RXR-α and VDR were higher in the healthy group and lower in the periodontitis and peri-implantitis groups. CONCLUSION: The results revealed that RXR-α and VDR levels were higher, while PPAR-γ and COX-2 levels were lower in the healthy group and periodontitis and peri-implantitis groups resulting in similar expressions in the tested parameters.

Effect of diabetes on collagen metabolism and hypoxia in human gingival tissue: a stereological, histopathological, and immunohistochemical study.

Diabetes mellitus and periodontitis are chronic inflammatory diseases that disrupt soft tissue metabolism. The diseases separately or together increase apoptosis in gingival fibroblast cells and reduce cell renewal. We investigated the effects of diabetes and periodontitis on the composition and structure of gingival connective tissue. We used gingival biopsies from 16 healthy individuals (control group, C), 16 type 2 diabetic patients with chronic periodontitis (diabetes + periodontitis group, D + P) and 16 healthy chronic periodontitis patients (periodontitis group, P). Biopsies were obtained under local anesthesia. Clinical attachment level (CAL), gingival index (GI) and plaque index (PI) were measured prior to gingival biopsies. Fibroblast cells were counted stereologically. Inflammatory cells were counted histomorphometrically. Hypoxia-inducible factor (HIF)-1α, lysyl hydroxylase (PLOD-2), neutrophil collagenase (MMP-8), and vascular endothelial growth factor (VEGF) levels were evaluated immunohistochemically. CAL, GI and PI for the C group were lower than for the other groups (p < 0.05). Fibroblast cell counts were lower for the D + P group than for the other groups (p < 0.05). Diabetes increased inflammatory cell numbers in the D and D + P groups compared to the C and P groups. MMP-8 levels were higher for the D + P group than for the other groups. VEGF was elevated in both the P and D + P groups compared to the C group, while HIF-1α and PLOD-2 levels were comparable. Diabetes increased tissue destruction and inflammation, and decreased fibroblast cell numbers without affecting collagen crosslinking and HIF-1α levels.

Effects of different bone marrow stimulation techniques on avascular zone meniscal defects.

OBJECTIVES: In this study, we sought to investigate the effect of different amounts of Bone Marrow-Derived Mesenchymal Stem Cells (BMSCs), obtained by different BMSCs, on the healing of avascular zone meniscal defects. BACKGROUND: Treating avascular zone meniscal injuries has gained popularity. BMSCs contribute to the healing of avascular zone meniscal defects. The amount of BMSCs derived from different bone marrow stimulation techniques (BMSTs) varies, which could affect the therapeutic efficacy of this treatment. METHODS: Fifty-four skeletally mature female New Zealand White rabbits were used after local ethical committee approval. A full thickness, 1.5 mm diameter defect was produced in the inner two-thirds of the anterior portion of the medial meniscus avascular zone using a biopsy punch. Animals were enrolled into three different groups according to BMST (0.8 mm, 1.5 mm, and 4 mm). Medial menisci were harvested and prepared for histomorphometric, histologic and immune-histologic analyses. RESULTS: Larger bridging tissues across the defect were detected in the 1.5-mm and 4-mm groups at 4 weeks (p < 0.05). The best quality score at the 1-,4- and 12-week endpoints was in 0.8 mm, 4 mm and 0.8 mm, 1.5 mm, respectively (p 0.05)CONCLUSION: The largest amount of BMSCs did not correlate with best quality and largest quantity of bridging tissue at the avascular zone in meniscal defects (Tab. 3, Fig. 4, Ref. 30).

Morphometric and histopathological evaluation of the effect of grape seed proanthocyanidin on alveolar bone loss in experimental diabetes and periodontitis.

OBJECTIVE: Grape seed proanthocyanidine extract (GSPE) is a strong antioxidant derived from the grape seeds (Vitis vinifera, Terral J.F.) and has a polyphenolic structure with a wide range of biological activity. The aim of the present study was to evaluate the effects of GSPE on alveolar bone loss and histopathological changes in rats with diabetes mellitus and ligature-induced periodontitis. MATERIAL AND METHODS: Forty rats were divided into 6 study groups. Control (C, 6 rats) group, periodontitis (P, 6 rats) group, diabetes (D, 6 rats) group, diabetes and periodontitis (D+P, 6 rats) group, diabetes, periodontitis and 100 mg/kg/day GSPE (GSPE-100, 8 rats), and diabetes, periodontitis and 200 mg/kg/day GSPE (GSPE-200, 8 rats) group. Diabetes mellitus was induced by intraperitoneal injection of a single dose of streptozotocin (60 mg/kg). Periodontitis was induced via ligation method. Silk ligatures were placed at the mandibular right first molars. GSPE was administered by oral gavage. After 30 days, all rats were killed. Alveolar bone loss was measured morphometrically via a stereomicroscope. For histopathological analyses, Alizarin red staining, and matrix metalloproteinase (MMP)-8, vascular endothelial growth factor and hypoxia inducible factor (HIF)-1α immunohistochemistry were performed. Tartrate-resistant acid phosphatase-positive osteoclast cells and relative total inflammatory cells were also determined. RESULTS: The highest alveolar bone loss was observed in the D+P group (P < .05). GSP-200 group decreased alveolar bone loss (P < .05). The D+P group had the highest osteoclast counts, but the difference was not significant compared to the P, GSPE-100 and GSPE-200 groups (P > .05). The inflammation in the D+P group was also higher than the other groups (P < .05). The osteoblast numbers increased in the GSPE-100 and GSPE-200 groups compared to the P and D+P groups (P < .05). MMP-8 and HIF-1α levels were highest in the D+P group and GSPE significantly decreased these levels (P < .05). CONCLUSION: Within the limits of this animal study, it can be suggested that GSPE administration may decrease periodontal inflammation and alveolar bone loss via decreasing MMP-8 and HIF-1α levels and increase osteoblastic activity in diabetic rats with experimental periodontitis.

The ameliorative effects of Ginkgo biloba on apoptosis, LH-R expression and sperm morphology anomaly in testicular torsion and detorsion.

Torsion/detorsion (T/D) induces testicular damages in both germinal epithelial and interstitial tissues. Ginkgo biloba extract (GbE) exerts antioxidant and free radical scavenger. We investigated the effect of GbE on testicular tissues, Leydig and sperm cells in rats injured with T/D. Twenty-eight Wistar albino rats were randomly assigned into four groups (Control, GbE, Treatment: T/D+GbE, T/D). T/D performed to the rats in torsion, treatment received GbE (50 mg/kg) 1 hr before T/D, GbE group received only GbE (50 mg/kg) and control was defined as sham group. After T/D, the testes along with epididymis were removed and processed. LH-R expression, apoptosis, sperm morphology and histopathological damage scores were determined for each group. Testicular T/D caused significant increases in apoptosis and sperm morphology anomaly, and a significant decrease in Johnsen's testicular biopsy scores, LH-R expression of Leydig cell and normal sperm cell count. GbE ameliorated testicular histopathology and caused significant increases in LH-R expression, normal sperm cell count in the treated and particularly GbE group. Consequently, GbE may prevent testicular injury and enhance Leydig and sperm cell activity following both T/D and normal situation owing to its antioxidant, anti-apoptotic, free radical scavenger and anti-inflammatory effects.

Investigation of the effect of astaxanthin on alveolar bone loss in experimental periodontitis.

BACKGROUND AND OBJECTIVE: Astaxanthin is a keto-carotenoid that has a strong antioxidant effect. The purpose of this study was to evaluate the effects of astaxanthin on alveolar bone loss and histopathological changes in ligature-induced periodontitis in rats. MATERIAL AND METHODS: Wistar rats were divided into four experimental groups: non-ligated (C, n = 6); ligature only (L, n = 6); ligature and astaxanthin (1 mg/kg/day astaxanthin, AS1 group, n = 8); ligature and astaxanthin (5 mg/kg/day astaxanthin, AS5 group, n = 8). Silk ligatures were placed at the gingival margin of lower first molars of the mandibular quadrant. The study duration was 11 days and the animals were killed at the end of this period. Changes in alveolar bone levels were clinically measured and tissues were immunohistochemically examined, osteocalcin, bone morphogenic protein-2, inducible nitric oxide synthase, Bax and bcl-2 levels in alveolar bone and tartrate-resistant acid phosphatase-positive osteoclast cells, osteoblast and inflammatory cell counts were determined. RESULTS: Alveolar bone loss was highest in the L group and the differences among the L, AS1 and AS5 groups were also significant (P < .05). Both doses of astaxanthin decreased tartrate-resistant acid phosphatase-positive+ osteoclast cell and increased osteoblast cell counts (P < .05). The inflammation in the L group was also higher than those of the C and AS1 groups were (P < .05) indicating the anti-inflammatory effect of astaxanthin. Although inducible nitric oxide synthase, osteocalcin, bone morphogenic protein-2 and bax staining percentages were all highest in the AS5 group and bcl-2 staining percentage was highest in the AS1 group, values were close to each other (P > .05). CONCLUSION: Within the limits of this study, it can be suggested that astaxanthin administration may reduce alveolar bone loss by increasing osteoblastic activity and decrease osteoclastic activity in experimental periodontitis model.

Inhibition by Egb761 of the effect of cellphone radiation on the male reproductive system.

OBJECTIVES: To determine the effects of Egb761 on testicular tissues and semen parameters in rats exposed to cellphone waves. BACKGROUND: EGb761 has antioxidant properties as a free-radical scavenger. Cellphone electromagnetic radiation (EMR) induces oxidative stress in cells. METHODS: Twenty-one Wistar albino male adult rats were divided into three groups (control, experimental, treatment), including seven rats in each. The experimental and treatment groups were exposed to cellphone EMR (0.96 W/kg) for six weeks (4 hrs/day). Egb761 (100 mg/kg/day) was also added to the treatment. Testes, epididymal semen and blood plasma were used for analysis. RESULTS: Exposure to cellular phone radiation resulted in a significant impairment in testicular morphometry and histological structure, reduction of total and motile sperm numbers and plasma testosterone level. Egb761 administration improved testicular damage and led to a marked increase in plasma testosterone levels and total and motile sperm numbers. CONCLUSION: Male reproductive system is susceptible to cellphone radiation. Cellphone waves induce toxic effects in testicular tissues, impair spermatogenesis and cause an imbalance in testosterone hormone levels. Egb761 ameliorated these toxic effects by reversing testicular tissue damage, restoring normal spermatogenesis and hormone levels. This suggests that Egb761 is a potential therapeutic agent against EMR-induced male reproductive toxicity (Tab. 3, Fig. 6, Ref. 45).