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With the rapid growth of China's economy since the reform and opening up, many industries have entered a period of rapid growth. Therefore, the macro environment at that time gave many industries the opportunity to develop. In the 1990s, the famous Chinese athlete Li Ning created the sports brand "Li Ning". Under the continuous improvement of the brand, Li Ning has become a world-famous sports brand after decades of development. Although Li Ning is a world-famous sports brand, its consumer group size still lags behind that of the world's top sports brands. This study found two solutions for Li Ning. First, create a co-brand. Second, increase the sponsorship of more influential events. This study puts forward some research methods for Li Ning. By strengthening the connection between the brand and consumers, Li Ning can have better fan effect, so as to achieve the purpose of expanding the international market. However, this study is only limited to the fans and brand linkage, and there are many aspects that are not discussed in this study.

Metabolic-associated fatty liver disease (MAFLD) is currently one of the main causes of chronic liver disease, but its potential mechanism remains unclear. This study proved that estrogen receptor α (ERα) could negatively control hepatocyte pyroptosis by inhibiting NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation, gasdermin D (GSDMD)-N generation, propidium iodide (PI) uptake, lactate dehydrogenase (LDH) release, and pro-inflammatory cytokine (IL-1β and IL-18) release. Furthermore, inhibition of pyroptosis ameliorated ERα deletion-induced metabolic dysfunction, insulin resistance, and liver injury. Mechanistically, ERα was confirmed to inhibit pyroptosis by directly interacting with GSDMD, and GSDMD blockade reversed the ERα inhibition-induced pyroptosis and improved lipid accumulation in hepatocytes. Notably, the treatment of wild-type (WT) mice with genistein, a phytoestrogen, could attenuate high-fat diet (HFD)-induced liver lipid steatosis and inhibit NLRP3-GSDMD-mediated pyroptosis. Results provide new insights into the underlying mechanism of pyroptosis regulation and uncover the potential treatment target of MAFLD.

Fumonisin B

The widespread application of bisphenols (BPs) has made them ubiquitous in the environment. Although the side effects of bisphenol A (BPA) substitutes have received increasing attention, studies on their reproductive toxicity remain lacking. In this research, the effects of BPA and its substitutes, including bisphenol S (BPS), bisphenol F (BPF), and bisphenol AF (BPAF), on the male reproductive system were evaluated. Results proved that these BPs disturbed germ cell proliferation, induced germ cell apoptosis, and perturbed sperm physiologies and spermatogenesis, which resulted from the disruption of testosterone (T) biosynthesis in Leydig cells (LCs). Importantly, in vitro and in vivo studies indicated that the exhausted cholesterol in LCs accounted for the reduced T production. Furthermore, the knockdown of peroxisome proliferator-activated receptor alpha (PPARα) remarkably ameliorated the downregulation of cholesterogenesis-related genes (i.e., Hmgcs1, Hmgcr, and Srebf2), indicating that PPARα played a critical role in BPs-induced testicular dysfunction. Overall, our studies indicated that BPS, BPF, and BPAF could induce testicular toxic effects similar to that of BPA, which were associated with the PPARα pathway.

Estrogen receptor β (ERβ) and NLRP6 are highly expressed in intestinal tissues. Loss of ERβ and NLRP6 exacerbate colitis in mouse models. However, the underlying mechanisms are incompletely understood. Here, we report that ERβ attenuates inflammation by inducing NLRP6-mediated autophagy. Specifically, ERβ directly activates the NLRP6 gene expression via binding to estrogen responsive element (ERE) of Nlrp6 gene promoter. ERβ also physically interacts with the NLRP6 nucleotide-binding domain and promotes NLRP6 inflammasome assembly. The ERβ-NLRP6 axis then interacts with multiple autophagy-related proteins including ULK1, BECN1, ATG16L1, LC3B, p62 to affect the autophagosome biogenesis and control autophagic flux. Finally, NLRP6-mediated autophagy suppresses the inflammatory response by promoting the K48-linked polyubiquitination of ASC, Casp-1 p20, IL-1β, TNF-α, and prohibitin-2. Thus, ERβ-NLRP6 direct an anti-inflammatory response by promoting autophagy. Our work uncovers an ERβ-NLRP6-autophagy pathway as an unrecognized regulatory mechanism that maintains intestinal epithelial cell homeostasis and facilitates tissue repair in colitis.

Bisphenol A (BPA) is an endocrine-disrupting chemical. Its influence on lipid homeostasis remains to be proven. In this study, the obese model of laying hens were induced using high-fat diet (HFD) to determine the lipid metabolism interference of BPA, especially its influence on estrogen receptors (ERs) and oxidative damage, at the dose of tolerable daily intake (TDI, 50 μg/kg body weight [BW]/day) and no observable adverse effect level (NOAEL, 5000 μg/kg BW/day). The results demonstrated that the TDI dose of BPA interacted with ERα more effectively than the NOAEL dose of BPA. The TDI dose of BPA increased the expression of ERα (esr1), which further changed the expression of lipid metabolism-related genes, such as cpt-1, lpl, creb1, and apov1. Furthermore, the abdominal fat rate, hematoxylin-eosin staining of adipocytes, and the average area of the hens were reduced. Therefore, the TDI dose of BPA played an estrogen-compensating role and weakened the effect of HFD on obesity in aged hens. By contrast, BPA at NOAEL dose exhibited great oxidative stress, which remarkably inhibited the activities of antioxidant-related enzymes (total superoxide dismutase and glutathione peroxidase) and promoted the excessive accumulation of lipid peroxidation products (malondialdehyde). Moreover, the increase in oxidative stress corresponded well with the increase in the expression of fat-forming genes (srebp-1, fas, acc, and ppar γ). That is, BPA at NOAEL may accelerate the process of fat formation.

Fowl adenovirus serotype 4 (FAdV-4) is the pathogen causing hepatitis-hydropericardium syndrome (HHS) in broilers. Since June 2015, it has emerged as one of the leading causes of economic losses in the poultry industry in China. Although most studies on FAdV-4 have focused on its pathogenicity to broilers, limited studies have been performed on other natural hosts such as ducks and geese. In this study, we assessed the pathogenicity of FAdV-4 to ducks of different ages through intramuscular injection and found that infected ducks showed severe growth depression. The infected ducks also suffered from extensive organ damage and had histopathological changes in the liver, spleen, and kidney. Although the virus infection caused lymphocyte necrosis of immune organs and the development of the bursa of Fabricius (bursa) was inhibited, the humoral immune response of infected ducks to FAdV-4 remained strong. The infected ducks also had high viral load in tissues and shed virus after the challenge. Overall, our research demonstrates that FAdV-4 can infect ducks and adversely affect the productivity of animals. And the viruses shed by infected ducks can pose a potential risk to the same or other poultry flocks.

Bisphenol A (BPA) and genistein (GEN) are selective estrogen receptor modulators, which are involved in the occurrence and development of metabolic syndrome. However, their roles in non-alcoholic fatty liver disease (NAFLD) of laying hens have not been reported. Here, we investigated the effects of different concentrations of GEN and BPA on the NAFLD of laying hens. Results showed that GEN ameliorated the high-energy and low-protein diet (HELP)-induced NAFLD by improving pathological damage, hepatic steatosis, and insulin resistance and blocking the expression of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-related factors. By contrast, high dose of BPA could aggravate these changes with serious symptom of NAFLD and suppress the level of ERα in the liver considerably, while GEN could reverse this phenomenon in a dose-dependent manner. In general, our research shows that the protective effect of GEN on NAFLD aims to improve the metabolic disorders and inflammation closely connected to ERα, while BPA can inhibit the expression of ERα and exacerbate the symptom of NAFLD. In conclusion, we elucidate the opposing effects of GEN and BPA in NAFLD of laying hens, thus providing a potential mechanism related to ERα and inflammation.

The reproductive toxicity of endocrine-disrupting chemicals has become a matter of great concern. However, the potential toxicological mechanism of typical environmental estrogens, bisphenol A (BPA) and genistein (GEN), on adult ovary remains ambiguous. In this study, we used laying hens as the experimental model and aimed to clarify the effect of long-term exposure to safe reference doses of BPA and GEN on adult ovary. Results demonstrated that 1/10 no-observable-adverse effect-level dose (1/10 NOAEL, 500 μg/kg body weight [bw]/day) of BPA significantly reduced the production performance and caused the degeneration of follicles and stromal cells and the increase of atretic follicles. Moreover, 1/10 NOAEL dose of BPA undermined the redox homeostasis of the ovary through activating Keap1 and suppressing the Nrf2-signaling pathway (Nrf2, NQO1, and HO-1). On the contrary, GEN (20, 40 mg/kg bw/day) dramatically improved the antioxidant capacity of the ovary by regulating the Nrf2-Keap1 pathway, enhancing the activities of antioxidant-related enzymes (CAT, GSH-Px, and T-SOD), and inhibiting the excessive accumulation of lipid peroxidation products (MDA). Parallel in vitro studies confirmed that the differential role of BPA and GEN on ovarian redox balance was directly mediated by Nrf2-Keap1 antioxidant system. And GEN could ameliorate BPA-induced oxidative stress. Importantly, our research found that exposure to BPA and GEN altered estrogen receptor alpha (ERα) expression in the ovary. And the use of specific ERα agonist/antagonist confirmed that BPA and GEN have opposite regulatory effects on the Nrf2-Keap1 pathway by targeting ERα.