Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in the world. Hydrogen sulfide (H2S) plays an important role in physiology and pathophysiology of liver. However, whether exogenous H2S could mitigate the hepatic steatosis in mice remains unclear. The aim of this study is to evaluate the effects of H2S on fatty liver. C57BL/6 mice were fed with either a high-fat diet (HFD) or a normal fat diet (NFD) for 16 weeks. After 12 weeks of feeding, the HFD-fed mice were injected one time per day with NaHS or saline for the followed 4 weeks. Compared to NFD, HFD could induce an accumulation of lipids in liver and a damage of hepatic structure. Compared to saline treatment, in the liver of HFD fed mice H2S treatment could significantly (1) recover the structure; (2) decrease the accumulation of lipids including triglyceride (TG) and total cholesterol (TC); (3) decrease the expression of fatty acid synthase (FAS) and increase the expression of carnitine palmitoyltransferase-1 (CPT-1); (4) reduce malondialdehyde (MDA) levels; (5) increase the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx). H2S could mitigate the fatty liver by improving lipid metabolism and antioxidant potential in HFD-induced obese mice.

Photodynamic therapy (PDT), a promising treatment modality, employs photosensitizers to generate cytotoxic reactive oxygen species (ROS) within localized tumor regions. This technique involves administering a photosensitizer followed by light activation in the presence of oxygen (O₂), resulting in cytotoxic ROS production. PDT’s spatiotemporal selectivity, minimally invasive nature, and compatibility with other treatment modalities make it a compelling therapeutic approach. However, hypoxic tumor microenvironment (TME) poses a significant challenge to conventional PDT. To overcome this hurdle, various strategies have been devised, including in-situ O₂ generation, targeted O₂ delivery, tumor vasculature normalization, modulation of mitochondrial respiration, and photocatalytic O₂ generation. This review aims to provide a comprehensive overview of recent developments in designing tumor-oxygenated nanomaterials to enhance PDT efficacy. Furthermore, we delineate ongoing challenges and propose strategies to improve PDT’s clinical impact in cancer treatment.

Metabolic syndrome is a chronic metabolic disorder that has turned into a severe health problem worldwide. A previous study reported that large yellow tea exhibited better anti-diabetic and lipid-lowering effects than green tea. Nevertheless, the potential mechanisms are not yet understood. In this study, we examined the prevention effects and mechanisms of large yellow tea water extract (LWE) on metabolic syndrome using leptin receptor knockout (Lepr^−/−) rats. Seven-week-old male Lepr^−/− and wild type (WT) littermate rats were divided into Lepr^−/− control group (KO) (n = 5), Lepr^−/− with LWE-treated group (KL) (n = 5), WT control group (WT) (n = 6), and WT with LWE intervention group (WL) (n = 6). Then, the rats were administered water or LWE (700 mg/kg BW) daily by oral gavage for 24 weeks, respectively. The results showed that the administration of LWE significantly reduced the serum concentrations of random blood glucose, total cholesterol, triglyceride, and free fatty acids, and increased glucose tolerance in Lepr^−/− rats. Moreover, LWE remarkably reduced hepatic lipid accumulation and alleviated fatty liver formation in Lepr^−/− rats. A mechanistic study showed that LWE obviously activated SIRT6 and decreased the expression of key lipogenesis-related molecules SREBP1, FAS, and DGAT1 in the livers of Lepr^−/− rats. Furthermore, LWE significantly improved microbiota dysbiosis via an increase in gut microbiota diversity and an abundance of the microbiota that produce short chain fatty acids (SCFAs), such as Ruminococcaceae, Faecalibaculum, Intestinimonas, and Alistipes. Finally, LWE supplementation increased the concentrations of SCFAs in the feces of Lepr^−/− rats. These results revealed that LWE attenuated metabolic syndrome of Lepr^−/− rats via the reduction of hepatic lipid synthesis through the SIRT6/SREBP1 pathway and the modulation of gut microbiota.

Huangshan Maofeng green tea (HMGT) is one of the most well-known green teas consumed for a thousand years in China. Research has demonstrated that consumption of green tea effectively improves metabolic disorders. However, the underlying mechanisms of obesity prevention are still not well understood. This study investigated the preventive effect and mechanism of long-term intervention of Huangshan Maofeng green tea water extract (HTE) on obesity-associated metabolic disorders in leptin receptor knockout (Lepr^−/−) rats by using gut microbiota and hepatic lipidomics data. The Lepr^−/− rats were administered with 700 mg/kg HTE for 24 weeks. Our results showed that HTE supplementation remarkably reduced excessive fat accumulation, as well as ameliorated hyperlipidemia and hepatic steatosis in Lepr^−/− rats. In addition, HTE increased gut microbiota diversity and restored the relative abundance of the microbiota responsible for producing short chain fatty acids, including Ruminococcaceae, Faecalibaculum, Veillonellaceae, etc. Hepatic lipidomics analysis found that HTE significantly recovered glycerolipid and glycerophospholipid classes in the liver of Lepr^−/− rats. Furthermore, nineteen lipid species, mainly from phosphatidylcholines (PCs), phosphatidylethanolamines (PEs), and triglycerides (TGs), were significantly restored increases, while nine lipid species from TGs and diglycerides (DGs) were remarkably recovered decreases by HTE in the liver of Lepr^−/− rats. Our results indicated that prevention of obesity complication by HTE may be possible through maintaining homeostasis of gut microbiota and certain hepatic lipid classes.

Obesity is a major public health concern globally. Plant-based ingredients have been proposed as alternative treatments for obesity. L-Theanine (THE), a unique nutraceutical component of tea, is known for its neuroprotective and cognitive benefits. However, there are few reports on THE’s effects and mechanisms in improving obesity and its complications. In this study, the alleviating effects and potential mechanisms of THE on obesity-related complications (ORCs) induced by a high-fat diet(HFD) in mice were explored by performing biochemical, hepatic transcriptomics, and plasma metabolomics analyses. The results indicated THE (900 mg/kg of body weight) was effective in mitigating ORCs by decreasing body weight gain and fat deposition, improving glycolipid metabolism disorders, inflammation dysregulation, and alleviating fatty liver formation due to long-term HFD. The hepatic transcriptomics data suggested that THE intervention suppresses the lipid metabolism and inflammation pathways in HFD-fed mice, thereby inhibiting hepatic steatosis and inflammation. Moreover, plasma metabolomics analysis revealed that THE exhibited positive effects on the homeostasis of plasma metabolite balance, such as phosphatidylcholine (PC(14:0/18:1)), phosphatidylethanolamine (Lyso-PE(14:0)), phosphatidic acid (PA(16:0e/18:0)), stigmasterol, and deoxycholic acid glycine conjugate. These metabolites were strongly correlated with ORC-related indicators. Our results indicated that THE, as a functional food additive, possesses potential for ORC alleviation. However, the exact molecular mechanism of how THE alleviates ORCs needs to be investigated in the future.

Background: Large yellow tea (LYT), a distinctive variety made from mature leaves, has recently gained attention for its remarkable health benefits. However, whether these benefits can be transmitted from mother to offspring remains unexplored. Purpose: This study investigated whether maternal LYT consumption confers cross-generational protection against metabolic and behavioral disorders induced by perinatal bisphenol A (BPA) exposure. Methods: A mouse model of perinatal BPA exposure (0.03% in diet) was established with or without maternal LYT supplementation (2.5% in diet). Metabolic parameters were assessed through biochemical assays and gene expression analysis (RT-PCR). Energy expenditure and spontaneous activity were monitored using a Comprehensive Lab Animal Monitoring System (CLAMS). Hippocampal proteomic profiling was performed using label-free quantitative proteomics. Results: LYT significantly reduced BPA absorption and enhanced its glucuronidation and excretion. Notably, LYT exhibited bidirectional metabolic regulation, alleviating gestational hyperglycemia in dams while restoring hypoglycemia in offspring, and normalizing underweight and hypolipidemia without disturbing normal physiology. Mechanistically, LYT modulated the SIRT6 (sirtuin 6)/FOXO1 and SIRT6/SREBP1 pathways to enhance gluconeogenesis and lipogenesis. Concurrently, LYT rectified BPA-induced hyperactivity and reduced energy expenditure. Proteomic analysis revealed that LYT partially restores BPA-induced dysregulation of cholesterol metabolism and glutamatergic/GABAergic synaptic pathways, rebalancing excitation-inhibition homeostasis. Conclusions: These findings establish LYT as a promising dietary intervention for counteracting environmental health risks across generations, acting through toxin clearance, bidirectional metabolic regulation, behavioral normalization, and neural excitation-inhibition balance restoration.