Assessing the impact of dental restorative materials on fibroblast cells: an immunohistochemical and ELISA analysis.

In this study, our aim was to investigate the effects of restorative materials such as composite, compomer and high viscosity glass ionomer, which are frequently used in dentistry, on L929 fibroblast cells by evaluating the oxidative stress parameters, pro- and anti-inflammatory cytokines, and apoptosis markers. L929 fibroblast cells were cultured, and dental filling materials were applied in two doses (50 and 100 µl). Immunohistochemical staining was performed for experimental groups with Anti-Bax and Anti-Caspase 9 antibodies. Then, ELISA technique was used to detect the level of TNF-alpha, TGF-beta, IL-1-beta, IL-6, IL-10, LPO and CAT. In the light of the data, the examined dental filling materials were effective on increasing the TGF-beta, IL-10, LPO and CAT levels, and decreasing the TNF-alpha, IL-1-beta, and IL-6 levels. The histological micrographs were also support the issues. When the levels of H-score in Caspase 9 labeled micrographs were evaluated, the mean of the control group was lower than the mean of the experimental groups. Biocompatibility varies according to the content of the material, the amount of residual monomer, and its solubility. Although all the experimental groups have cytotoxic effects, the least effect is seen in the Omnichroma group.

The effects of cisplatin and jaceosidin on SH-SY5Y neuroblastoma cells: an electron microscopic, molecular and biochemical study.

In this study, our aim was to show both the single and combined effects of cisplatin and jaceosidin in SHSY-5Y neuroblastoma cells. For this purpose, we used MTT cellular viability assay, Enzyme-Linked Immunosorbent Assay (ELISA), Transmission Electron Microscopy (TEM), Immunofluorescence Staining Assay (IFA) and Western blotting (WB) assay. According to MTT findings, IC50 dose was detected as 50 µM cisplatin and 160 µM jaceosidin co-application. Therefore, experimental groups were finally selected as control, cisplatin, 160 µM jaceosidin and Cisplatin +160 µM jaceosidin. Cell viability was decreased in all groups, and the IFA findings confirmed the viability analysis. WB data indicated that matrix metalloproteinase 2 and 9 levels, as indicators of metastasis, decreased. While LPO and CAT levels increased in all treatment groups, it was observed that the activity of SOD decreased. When TEM micrographs were investigated, cellular damages were determined. In the light of these results, it can be said that cisplatin and jaceosidin have a potential to increase the effects of each other synergistically.

Two flavonoids, baicalein and naringin, are effective as anti-inflammatory and anti-oxidant agents in a rat model of polymicrobial sepsis.

INTRODUCTION: In this study, our aim was to investigate the possible protective and therapeutic effects of these two flavonoids, baicalein, and naringin, in 50 and 100 mg/kg doses applied both before and after cecal ligation and puncture (CLP) procedures in a polymicrobial sepsis rat model, and evaluate the possible contribution of oxidative and inflammatory markers by immunological, biochemical, molecular, and histopathological methods. METHODS: Sixty-six Wistar albino rats were divided into 11 groups. The pro-inflammatory (TNF-alpha, IL-1-beta, and IL-6) and anti-inflammatory (TGF-beta and IL-10) cytokine levels were measured by ELISA technique. CD3, CD68, and nuclear factor kappa B positivity rates were detected by immunohistochemical methods. Oxidative stress parameters (MDA, SOD, and GSH) were measured by tissue biochemistry. RESULTS: Sepsis caused a significant increase in all pro-inflammatory cytokine levels and MDA activity. Also, it led to an increase in the positivities of CD3, CD68, and NF-κB markers. However, especially pre-CLP doses of baicalein and naringin inhibited the inflammation process by suppressing pro-inflammatory and increasing anti-inflammatory cytokine levels, as well as regulating the oxidative stress process by normalizing the oxidant/anti-oxidant enzyme levels. CONCLUSION: Both pre- and post-application of baicalein and naringin are quite effective to prevent sepsis-caused cellular processes. This protective and therapeutic effects by baicalein and naringin in animals with sepsis seems to be originated from the high antioxidant capacity and inhibition of pro-inflammatory cytokine production. Thus, those natural agents may prove to be valuable protective agent against septic shock.

Anti-oxidant and anti-inflammatory effects of apigenin in a rat model of sepsis: an immunological, biochemical, and histopathological study.

OBJECTIVE: We hypothesize that apigenin may inhibit some cellular process of sepsis-induced spleen injury and simultaneously improve inflammation and oxidative stress. Therefore, the aim of this study was to investigate the potential protective effects of apigenin in a polymicrobial sepsis rat model of by cecal ligation and puncture. MATERIALS AND METHODS: 64 female Wistar albino rats were divided into 8 groups. The pro-inflammatory (tumor necrosis factor-alpha, interleukin-6, and interleukin-1-beta) and anti-inflammatory (tumor growth factor-beta and interleukin-10) cytokine levels were measured by enzyme-linked immunosorbent assay. CD3, CD68, and nuclear factor kappa B (NF-κB) positivity rates were detected by immunohistochemical methods. Oxidative stress parameters were measured by tissue biochemistry. RESULTS: Sepsis caused a significant increase in TNF-alpha, IL-1-beta, IL-6, and TGF-beta levels whereas it reduced IL-10 level. Additionally, it led to an increase in CD3, CD68, and NF-κB positivity rates as well as oxidative stress parameters levels. However, apigenin inhibited the inflammation process, increased the IL-10 level and normalized the oxidative stress parameters. DISCUSSION AND CONCLUSION: Pretreatment with apigenin results in a significant reduction in the amount of inflammatory cells. The beneficial effect of apigenin on spleen injury also involved inhibition of NF-κB pathway, suppression of proinflammatory cytokines, and induction of anti-inflammatory cytokine production. Additionally, it led to a decrease in oxidative stress in spleen tissue. Taking everything into account, apigenin may be an alternative therapeutic option for prevention of sepsis-induced organ.

Investigation of Helicobacter pylori antigen in stool samples of patients with upper gastrointestinal complaints.

Helicobacter pylori infection is usually acquired in early childhood and it can persist throughout life without antibiotic treatment. This study aimed to compare the accuracy of the noninvasive H. pylori Stool Antigen Test-applied on the stool samples with the invasive gold standart Rapid Urease Test-applied on the gastric biopy samples of patients with upper gastrointestinal complaints. After endoscopy, biopsy and stool specimens were taken in 122 patients. The infection was detected with rapid urease test which is accepted as gold standart test. Rapid, one-step H. pylori card test was applied to all patients stool specimens. In this study 106 of the 122 patients (86.8%) were positive for H. pylori infection, while 16 of the 122 patients (13.2%) were negative. H. pylori card test was negative in 13 of the 16 patients and was positive in 98 of the 106. The sensitivity, specifity, positive and negative predictive values were 92.45%, 81.25%, 97.02%, and 61.90%, respectively. H. pylori card test is rapid, easy, noninvasive and inexpensive methods for detection H. pylori infection. This test showed high sensitivity and specificity. Additionally, it may be a good alternative to invasive tests for the detection of H. pylori infections especially in children.

The protective effects of beta-carotene against ischemia/reperfusion injury in rat ovarian tissue.

INTRODUCTION: Beta-carotene is a well-known antioxidant and precursor of Vitamin A that has a preventative role in the oxidative damage process. Our aim was to investigate the possible preventive effects of beta-carotene on oxidative damage via experimental ischemia and ischemia-reperfusion models in rat ovaries. MATERIALS AND METHODS: A traumatic vascular clamps were used for 3h to induce ischemia (Group 2, 3, 4, 5, 6, 7). The clamps were then removed to allow reperfusion for 3h (Group 3, 6, 7). Sham-operated rats (Group 1) underwent laparotomy without the induction of ischemia/reperfusion injury. Real-Time-PCR was performed to determine IL-1-beta, IL-6 and iNOS expression levels. Histopathological (H&E) and immunohistochemical staining (NF-kß p65) processes were then performed. Finally, SOD, GSH, and MDA levels were determined. RESULTS: Intense hemorrhagic areas were observed in both the ischemia and ischemia/reperfusion groups, whereas minimal hemorrhage was observed in the treatment groups. The ischemia and ischemia/reperfusion groups exhibited extreme immunoreactivity, detected by NF-kß p65 staining; this reactivity decreased after the application of beta-carotene. The expression of IL-1-beta, IL-6, and iNOS in the injury groups increased significantly, whereas a dose-dependent improvement was observed in the treatment groups. Finally, MDA levels increased significantly and SOD and GSH levels decreased drastically in the injury groups. However, these values obtained from I/R groups were normalized after beta-carotene treatment. DISCUSSION: In this study, we demonstrated via molecular and biochemical parameters the protective effect of beta-carotene, which is a potent antioxidant, on the experimental ischemia-reperfusion model.

Hepatoprotective effect of 17ß-estradiol as antioxidant modulators against stress damage.

BACKGROUND: Liver is one of the most important organs affected by exercise. According to the literature a few study to date has investigated the effects of estrogen supplementation on exercise-induced oxidative stress in liver tissue of rats. OBJECTIVES: We aimed to investigate the effects of estrogen supplementation on oxidative stress markers in liver tissue of exercised rats. MATERIALS AND METHODS: Male rats (n = 35) were divided as estrogen supplemented (n = 18) and non-supplemented groups (n = 17); these groups were further divided as rest and eccentric exercised groups. Eccentric exercise groups were further divided as rats killed after 1 hour and 48 hours of eccentric exercise. Estrogen (10 mg/kg) was administered subcutaneously for 30 days. Eccentric exercise was applied as treadmill run (15° downhill, 20 m/min) consisting of periods of "5 min" run and 2 min rest repeated 18 times. The rat liver was examined biochemically and histologically. Activities of GST, GSH-Px, CAT, SOD and MDA concentration were also measured spectrophotometrically. RESULTS: Some disruptions were detected in experimental groups compared with the control group. Additionally, exercise training caused an increase in SOD and decrease in GSH-Px activities in some experimental groups. SOD activities increased significantly in group 3 (Estrogen (-), eccentric exercise (+) killed (after 1 h), compared with group 5 (Estrogen (-), eccentric exercise (+) killed (after 48 h). On the other hand, GSH-Px activities were also significantly decreased in groups 3, 4 and 5 compared with the control group. Leukocyte infiltration in liver increased after 48 hours compared with after 1 hour and estrogen supplementation was not able to prevent this infiltration. CONCLUSIONS: Estrogen seemed to be not very effective to prevent eccentric exercise-induced liver damage.