A significant association of inflammation grade with the number of LCs in OKCs is found. The paucity of finding LCs in the lining epithelia of OKCs without inflammation indicates the loss of immunosurveillance ability against the OKC lining epithelial cells; this can explain why OKCs have aggressive clinical behavior, a great growth potential, and a high recurrence rate.

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Scope Parkinson's disease is one of the neurodegenerative diseases that have no cure. Excitotoxicity induced by excess glutamate is known to be a hallmark of these diseases. Therefore, this study aims to evaluate the preventive effect of piceatannol on glutamate‐induced neurodegeneration via mitochondrial rescue. Methods and results The PC12 cell line and three Caenorhabditis elegans (C. elegans) strains are employed to achieve the aim. In the in vitro study, the results show that piceatannol can prevent glutamate‐induced apoptosis. Piceatannol also reduces mitochondrial reactive oxygen species (ROS) accumulation by activating the antioxidant system. Moreover, piceatannol can also promote mitochondrial biogenesis and induced mitochondrial fusion‐related genes to preserve mitochondrial functionality. In the C. elegans model, piceatannol can prevent mitochondrial fragmentation induced by glutamate. More importantly, piceatannol effectively protects dopaminergic neurons from degradation and preserves the responses controlled by these neurons. Conclusion The findings suggest that piceatannol can be a more effective and potent candidate for the treatment of neurodegenerative diseases, such as Parkinson's disease, compared to resveratrol. It is capable of preventing neurodegeneration induced by excess glutamate, possibly via mitochondrial rescue. It is recommended that piceatannol be developed into a neuroprotective agent.

Background: Obesity is associated with increased tissue and systemic inflammation and oxidative stress. Several experimental and epidemiological studies have demonstrated that acetaminophen has been associated with elevated levels of oxidative stress, which also causes impaired liver functions. The aim of this study is to evaluation of the effect of acetaminophen-induced changes of cytokines and oxidative stress in normal and high-fat diet (HFD)-induced obese rats. Methods: 48 male Wistar rats were randomly divided into six groups: (1) normal diet (ND); (2) ND-low doseacetaminophen (NLDA); (3) ND-high dose-acetaminophen (NHDA); (4) high-fat diet (HFD) (HFD-induced obese rats for 8 weeks); (5) HFD-low dose-acetaminophen (HLDA); (6) HFD-high dose-acetaminophen (HHDA) for 2 weeks. Growth parameters, weights of organ and adipose tissues, serum biochemical parameters, and oxidative stress were measured in normal and obese rats intake various doses of acetaminophen. Results: The data indicated that body weight, perirenal adipose tissue, and epididymal adipose tissue in HFD-low doseacetaminophen (HLDA) and HFD-high dose-acetaminophen (HHDA) groups were significantly decreased as compared to the HFD group. Serum parameter levels of total cholesterol, LDL-cholesterol, aspartate aminotransferase, alanine aminotransferase, interleukin-6, and interleukin-1β in HHDA group was significantly increased as compared to the HFD group. The serum parameter levels of alanine aminotransferase and aspartate aminotransferase in HHDA group was significantly increased as compared to the NHDA group. In the trolox equivalent antioxidant capacity (TEAC) and malondialdehyde (MDA), hepatic TEAC in HLDA and HHDA groups were significantly decreased as compared to the HFD group. Moreover, hepatic and serum levels of MDA in HHDA group was significantly increased as compared to the HFD group. In the hepatic antioxidant enzymatic activities, the levels of glutathione, glutathione reductase, and catalase in HHDA group was significantly decreased as compared to the HFD group. The pathological results show that the scores of portal inflammation and intralobular degeneration and inflammation in HLDA and HHDA groups were significantly increased as compared to NLDA and NHDA groups. These results demonstrated that the intake of acetaminophen can enhance oxidative stress and cause impaired liver functions in rats fed a high-fat diet.