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Background: Amphibians decline globally due to infection with virulent bacteria, despite their vital roles in the ecosystem. The current study aimed at addressing the pathological and bacterial findings of the infected Pelophylax ridibundus indigenous to the Al‐Ahsa region. Many clinical signs were observed in the eggs, including discoloration, disintegration of the outer jelly coat; defects in morphology, and mortality were reported. Furthermore, neuromasts lacking apical cilia and microvilli were observed in the cleavage stages of the infected developing egg. Additionally, cutaneous hyperaemia, lethargy, peripheral oedema, subcutaneous haemorrhage and cutaneous ulcerations were observed in the infected P. ridibundus adults. Methods: Ribbons of frog eggs were collected from Al‐Ahsa oasis, the Eastern region, Kingdom of Saudi Arabia (KSA), and examined under light and scanning electron microscope. The developed eggs and adults were further examined using a dissecting microscope to determine signs of infection. A bacterial strain designated as PRE‐1 was isolated from the infected eggs, identified genotypically and then characterized phenotypically. Strain PRE‐1 was identified as Aeromonas hydrophila based on the comparative gene sequences of the 16S rRNA gene at identity level of (99.92%). Furthermore, phylogenetic relationship based on the 16S rRNA gene sequences of our strain and other relevant strains Aeromonas spp. showed that PRE‐1 formed a cluster with A. hydrophila (99% bootstrap support), providing a robustness to the identification of PRE‐1 as A. hydrophila. This bacterium was found to be associated with disease outbursts in the marsh frogs from the Al‐Ahsa region. Conclusion: It is important to continue monitoring the emerging diseases so that their cause can be discerned, and appropriate protocols can be applied to limit the spread of the loss of amphibians, which are vital for our ecosystem. [ABSTRACT FROM AUTHOR]

In this study, kaempferol (KFL) shows hepatoprotective activity against zearalenone (ZEA)-induced oxidative stress and its underlying mechanisms in in vitro and in vivo models were investigated. Oxidative stress plays a critical role in the pathophysiology of various hepatic ailments and is normally regulated by reactive oxygen species (ROS). ZEA is a mycotoxin known to exert toxicity via inflammation and ROS accumulation. This study aims to explore the protective role of KFL against ZEA-triggered hepatic injury via the PI3K/Akt-regulated Nrf2 pathway. KFL augmented the phosphorylation of PI3K and Akt, which may stimulate antioxidative and antiapoptotic signaling in hepatic cells. KFL upregulated Nrf2 phosphorylation and the expression of antioxidant genes HO-1 and NQO-1 in a dose-dependent manner under ZEA-induced oxidative stress. Nrf2 knockdown via small-interfering RNA (siRNA) inhibited the KFL-mediated defence against ZEA-induced hepatotoxicity. In vivo studies showed that KFL decreased inflammation and lipid peroxidation and increased H2O2 scavenging and biochemical marker enzyme expression. KFL was able to normalize the expression of liver antioxidant enzymes SOD, CAT and GSH and showed a protective effect against ZEA-induced pathophysiology in the livers of mice. These outcomes demonstrate that KFL possesses notable hepatoprotective roles against ZEA-induced damage in vivo and in vitro. These protective properties of KFL may occur through the stimulation of Nrf2/HO-1 cascades and PI3K/Akt signaling. [ABSTRACT FROM AUTHOR]

D-galactose (D-gal) administration was proven to induce cognitive impairment and aging in rodents' models. Geraniol (GNL) belongs to the acyclic isoprenoid monoterpenes. GNL reduces inflammation by changing important signaling pathways and cytokines, and thus it is plausible to be used as a medicine for treating disorders linked to inflammation. Herein, we examined the therapeutic effects of GNL on D-gal-induced oxidative stress and neuroinflammation-mediated memory loss in mice. The study was conducted using six groups of mice (6 mice per group). The first group received normal saline, then D-gal (150 mg/wt) dissolved in normal saline solution (0.9%, w/v) was given orally for 9 weeks to the second group. In the III group, from the second week until the 10th week, mice were treated orally (without anesthesia) with D-gal (150 mg/kg body wt) and GNL weekly twice (40 mg/kg body wt) four hours later. Mice in Group IV were treated with GNL from the second week up until the end of the experiment. For comparison of young versus elderly mice, 4 month old (Group V) and 16-month-old (Group VI) control mice were used. We evaluated the changes in antioxidant levels, PI3K/Akt levels, and Nrf2 levels. We also examined how D-gal and GNL treated pathological aging changes. Administration of GNL induced a significant increase in spatial learning and memory with spontaneously altered behavior. Enhancing anti-oxidant and anti-inflammatory effects and activating PI3K/Akt were the mechanisms that mediated this effect. Further, GNL treatment upregulated Nrf2 and HO-1 to reduce oxidative stress and apoptosis. This was confirmed using 99m Tc-HMPAO brain flow gamma bioassays. Thus, our data suggested GNL as a promising agent for treating neuroinflammation-induced cognitive impairment.