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ObjectiveCisplatin (CDDP) has been known to be an effective antineoplastic drug; however, it has a cardiotoxic effect. Curcumin (CMN) and beta-carotene (BC) have been suggested to protect biological systems against CDDP-induced damage. The current study was conducted to evaluate the possible protective roles of CMN and BC on CDDP-induced cardiotoxicity in rat cardiac tissues.MethodsA total of 49 adult femaleWistar albino rats were equally divided into seven groups as followscontrol (no medication), sesame oil (1 mg/kg), CDDP (single dose injection two times as once a week, 5 mg/kg/week), BC (100 mg/kg), CDDP+BC (pretreated BC for 30 min before CDDP injection), CMN (200 mg/kg), and CDDP+CMN (pretreated CMN for 30 min before CDDP injection). These treatments were applied intraperitoneally for CDDP and with gavage for CMN and BC. The oxidative/antioxidant indicators, inflammatory cytokines, and histopathological alterations were examined.ResultsThese alterations included a marked increase in malondialdehyde (MDA) level, significant decrease in catalase (CAT) and superoxide dismutase (SOD) activities, and significant elevation of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, interleukin (IL)-6 in the CDDP group compared with the other groups. Histopathologically, CDDP-induced severe myocardial degenerative changes were observed. However, the CDDP-induced disturbances in the above-mentioned parameters significantly improved by treatment with BC and particularly CMN.ConclusionThis study indicated that CDDP treatment markedly caused cardiotoxicity; however, treatment with CMN or BC ameliorated this cardiotoxicity in rats. Furthermore, these findings revealed that treatment with CMN has a higher cardioprotective effect than that with BC against CDDP-induced cardiotoxicity in rat cardiac tissues.

Background: Bisphenol A (BPA) is one of the most commonly produced chemicals in the world. BPA is used in products such as food packaging, personal care products, detergents, and plastic bottles. This study was conducted to determine the effect of BPA on fetal bone development. Material and methods: In this study, 16 pregnant female Sprague-Dawley rats were used. The rats were divided into four groups: the control group and 0.5 mg/kg/day, 5 mg/kg/day, and 50 mg/kg/day dose BPA groups. The skeletal system development of fetuses was examined with double skeletal and immunohistochemistry (IHC) staining (tartrate resistant acid phosphatase (TRAP) and the alkaline phosphatase (AP) expressions) methods. Results: The highest ossification rates in the humerus, radius, and ulna were detected as 41.05%, 39.25%, and 37.26% in the control group, respectively. The highest ossification rates in the femur, tibia, and fibula were detected as 23.04%, 30.73%, and 32.78% in the control group, respectively. Statistically significant differences were found between control and experimental groups in the TRAP and AP expression of the femur by IHC staining (p < 0.001). Conclusion: Exposure to BPA during pregnancy adversely affected ossification and bone growth. A dosedependent decrease was observed in the rate of ossification.

AIM: Cornus mas L is commonly used due to its anti-infl ammatory, anti-carcinogenic and anti-oxidant properties. In the study, the effects of C. mas L extract on a solid tumor were examined in the Ehrlich solid tumor model developed in Balb/C type mice. METHODS: Ehrlich acid tumor (EAT) cells (1x10 6 EAT cell) from the stock animal were injected subcutaneously (s.c.) through the nape of the mice. Treatment groups of solid tumor-induced animals received 100 mg/kg and 200 mg/kg of C. mas L extract intraperitoneally (i.p.) for 14 days. RESULTS: Tumor volumes and animal weights were found to be statistically signifi cant compared to the control group (p < 0.05). AgNOR staining was performed in tumor tissues. Statistically signifi cant differences were observed between the groups in terms of TAA/NA ratio (p < 0.05). Immunohistochemical and biochemical parameters were also evaluated. An estimation of tumor proliferation of the lung, liver, brain, kidney, testis and tumor antioxidant parameters viz. lipid peroxidation, reduced glutathione (GSH), glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT) was made. CONCLUSIONS: Our study showed that the anti-tumor effect of C. mas L in assisted tumor development with EAT cells, was mediated by the enhancement of oxidative stress with multiple mechanisms (Tab. 6, Fig. 12, Ref. 38).

Background/aim Acute lung injury (ALI) is a major cause of death in the intensive care unit. Lipopolysaccharide (LPS) induced lung injury is the most widely used experimental ALI model and provides opportunities for new targeting therapy. In this study, we investigated the effects of tocilizumab, adalimumab, and methylprednisolone in LPS-induced acute lung injury. Materials and methods Lung injury was established by intratracheal instillation of LPS. The rats were randomly divided into six groups: LPS, control, and treatment groups (adalimumab, tocilizumab, methylprednisolone, adalimumab + tocilizumab). Bronchoalveolar lavage (BAL) and lung tissues were collected at 48 h and 96 h following LPS administration from each group. For histological analysis, hematoxylin–eosin (H&E) staining was performed. The sections were obtained for immunohistochemical analysis. IL-6 and TNF-alpha immunoreactivity were measured. Results Intratracheal LPS application resulted in inflammatory cell infiltration of interstitial and alveolar spaces and thickening of the alveolar wall. All treatment groups showed significantly amelioration compared to LPS at 48 h. Interestingly, adalimumab and adalimumab + tocilizumab groups showed a significant amelioration of the lung histoarchitecture, compared to the prednisolone group at 96 h (p = 0.028, p = 0.025, respectively). Compared to the control group, LPS stimulation resulted in a significant increase in IL-6 and TNF-alpha immunoreactivity (p < 0.001). IL-6 and TNF-alpha expression were markedly reduced in all treatment groups at 48 h but the reduction was greater in the adalimumab and tocilizumab group than in the steroid. Administration with adalimumab and/or tocilizumab effectively decreased expression of TNF-alpha (p = 0.001) and IL-6 (p < 0.001) at 96 h, but prednisolone did not exert an effective decrease (p > 0.05). Conclusion Adalimumab and/or tocilizumab significantly reduce the release of proinflammatory cytokines and improve the tissue inflammation in the experimental model of ALI. Our results suggest that adalimumab and/or tocilizumab have a more potent antiinflammatory effect on lung injury than the steroid.