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Nobiletin is a natural flavonoid found in citrus fruits with beneficial effects, including anti-inflammatory, anti-cancer and anti-oxidation effects. The aim of this study was to investigate whether nobiletin improves mitochondrial function in porcine oocytes and examine the underlying mechanism. Oocytes enclosed by cumulus cells were cultured in TCM-199 for 44 h with 0.1% dimethyl sulfoxide (control), or supplemented with 5, 10, 25, and 50 μM of nobiletin (Nob5, Nob10, Nob25, and Nob50, respectively). Oocyte maturation rate was significantly enhanced in Nob10 (70.26 ± 0.45%) compared to the other groups (control: 60.12 ± 0.47%; Nob5: 59.44 ± 1.63%; Nob25: 63.15 ± 1.38%; Nob50: 46.57 ± 1.19%). The addition of nobiletin reduced the levels of reactive oxygen species and increased glutathione levels. Moreover, Nob10 promoted mitochondrial biogenesis by upregulating the protein levels of sirtuin 1 (SIRT1) and peroxisome proliferator-activated receptor-gamma coactivator 1 α (PGC-1α). This resulted in an increase in the number of active mitochondria, mitochondrial DNA copy number, mitochondrial membrane potential, and ATP production, thereby enhancing mitochondrial function. The protein level of p53 decreased, followed by the phosphorylation of B-cell lymphoma 2, suggesting a reduction in mitochondria-mediated apoptosis in the Nob10 group. Additionally, the release of cytochrome c from the mitochondria was significantly diminished along with a decrease in the protein expression of caspase 3. Thus, nobiletin has a great potential to promote the in vitro maturation of porcine oocytes by suppressing oxidative stress and promoting mitochondrial function through the upregulation of the SIRT1/PGC-1 α signaling pathway. • Nobiletin enhanced meiotic maturation in porcine oocytes. • Nobiletin reduced oxidative stress during oocyte maturation. • Nobiletin promoted mitochondrial function by regulating SIRT1/PGC-1α signaling pathway in porcine oocytes. • Nobiletin attenuated apoptosis by inhibiting p53/Bcl-2 signaling pathway in porcine oocytes. [ABSTRACT FROM AUTHOR]

Influenza virus infection can cause kidney damage. However, the link between influenza infection and disease is still unclear. The purpose of this study was to analyze the relationship between heterophilic epitopes on H5N1 hemagglutinin (HA) and disease. The monoclonal antibody (mAb) against H5N1 was prepared, mAbs binding to human kidney tissue were screened, and the reactivities of mAbs with five different subtypes of influenza virus were detected. Design and synthesize the peptides according to the common amino acid sequence of these antigens, and analyze the distribution of the epitope on the crystal structure of HA. Immunological methods were used to detect whether the heterophilic epitopes could induce the production of antibodies that cross-react with kidney tissue. The results showed that H5-30 mA b binding to human kidney tissue recognized the heterophilic epitope 191-LVLWGIHHP-199 on the head of HA. The key amino acid were V192, L193, W194 and I196, which were highly conserved in human and avian influenza virus HA. The heterophilic epitope could induce mice to produce different mAbs binding to kidney tissue. Such heterophilic antibodies were also detected in the serum of the patients. It can provide materials for the mechanism of renal diseases caused by influenza virus infection. • H5-30 mA b binding to human kidney tissue recognized the heterophilic epitope 191-LVLWGIHHP-199 on the head of HA. • The key amino acid were V192, L193, W194 and I196, which were highly conserved in human and avian influenza virus HA. • The heterophilic epitope could induce mice to produce different mAbs binding to kidney tissue. • Such heterophilic antibodies were also detected in the serum of the patients. [ABSTRACT FROM AUTHOR]

Spinal cord injury (SCI) is a debilitating condition that is frequently accompanied by neuropathic pain, resulting in significant physical and psychological harm to a vast number of individuals globally. Despite the high prevalence of neuropathic pain following SCI, the precise underlying mechanism remains incompletely understood. Microglia are a type of innate immune cell that are present in the central nervous system (CNS). They have been observed to have a significant impact on neuropathic pain following SCI. This article presents a comprehensive overview of recent advances in understanding the role of microglia in the development of neuropathic pain following SCI. Specifically, the article delves into the detrimental and protective effects of microglia on neuropathic pain following SCI, as well as the mechanisms underlying their interconversion. Furthermore, the article provides a thorough overview of potential avenues for future research in this area. [ABSTRACT FROM AUTHOR]