Apilarnil is a bee product that has attracted attention due to its beneficial biological properties recently. This study aimed to investigate the effect of apilarnil (API) on endotoxin-induced lung injury. For the study, 64 adult male Sprague dawley rats were divided into eight groups; control, 0.2, 0.4 and 0.8 g / kg API treated groups by gavage for 10 days, 30 mg / kg lipopolysaccharide (LPS) administered intraperitoneally (single dose), LPS + 0.2, LPS + 0.4 and LPS + 0.8 g / kg API applied groups. In histopathological evaluation, hyperemia, intra-alveolar hemorrhage, cellular infiltration, and increased cellular abnormal proliferation were observed in the lung samples of the LPS group. It was found that the lung samples of LPS + 0,4 and LPS + 0,8 API groups decreased statistically significant compared to the LPS group. The number of TUNEL positive cells observed in both LPS and API treated groups showed a statistically significant decrease compared to the LPS group. In comet test, 0,8 API group was found to be reduced more in tail % DNA and tail length when LPS + API treated groups were compared with LPS group. In conclusion, the API applied to rats can prevent LPS-induced lung injury.

Diabetes mellitus (DM) has profound effects on the female mammalian reproductive system, and early embryonic development, reducing female reproductive outcomes and inducing developmental programming in utero. However, the underlying cellular and molecular mechanisms remain poorly defined. Accumulating evidence implicates endoplasmic reticulum (ER)-stress with maternal DM associated pathophysiology. Yet the direct pathologies and causal events leading to ovarian dysfunction and altered early embryonic development have not been determined. Here, using an in vivo mouse model of Type 1 DM and in vitro hyperglycaemia-exposure, we demonstrate the activation of ER-stress within adult ovarian tissue and pre-implantation embryos. In diabetic ovaries, we show that the unfolded protein response (UPR) triggers an apoptotic cascade by the co-activation of Caspase 12 and Cleaved Caspase 3 transducers. Whereas DM-exposed early embryos display differential ER-associated responses; by activating Chop in within embryonic precursors and Caspase 12 within placental precursors. Our results offer new insights for understanding the pathological effects of DM on mammalian ovarian function and early embryo development, providing new evidence of its mechanistic link with ER-stress in mice.

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Ovarian ischemia is a gynecological emergency case that occurs as a result of ovarian torsion. Oxidative stress plays a central role in the development of ischemia/reperfusion (IR) injuries. Lycopene (LYC) is a lipophilic, natural carotenoid well known for its antioxidant properties. This study provides information on the potential applications of lycopene. The Wistar Albino rats were distributed into six groups: Sham group (only a laparotomy was performed), Control group [laparotomy and intraperitoneal dissolvent (olive oil)], IR group, IR+olive oil group, IR+LYC 2.5 mg/kg/dose, intraperitoneal group, IR+LYC 5 mg/kg/dose intraperitoneal group. Evaluated in terms of histopathological changes, tissue malondialdehyde levels (MDA), ovarian expressions of phosphorylated nuclear factor-kappa B (p-NF-κB) and the TUNEL method was utilized to show apoptosis of ovarian tissue. There was a significant decrease in MDA, p-NF-κB values and the proportion of apoptotic cells assessed by TUNEL compared to the group that did not receive intraperitoneal LYC in rat injury with IR damage (P<0.05). In histopathological damage scoring, it was observed that the cell damage was significantly reduced in LYC-administered groups. LYC showed significant ameliorative effects on ovary injury caused by IR through acting as an antioxidant, antiinflammatory, and antiapoptotic agent.

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