Hydrogen sulfide therapy: a narrative overview of current research and possible therapeutic implications in future.

Diabetic nephropathy is one of the most important comorbidities in the diabetic population. In China, more and more young patients are showing an increasing prevalence of diabetes. As a gas molecule, hydrogen sulfide (H2 S) has some unique chemical and physiological functions. In recent years, it has been studied in various fields. These effects are manifested in the induction of renal vasodilation and anti-renal vascular fibrosis. The ball clearing function is improved. Therefore, increasing prospective studies have focused on how H2 S protects diabetic nephropathy and how to obtain H2 S by modern means to treat diabetic nephropathy.

Potential rules of anesthetic gases on glioma.

Glioma is one of the most frequent primary brain tumors. Currently, the most common therapeutic strategy for patients with glioma is surgical resection combined with radiotherapy or/and adjuvant chemotherapy. However, due to the metastatic and invasive nature of glioma cells, the recurrence rate is high, resulting in poor prognosis. In recent years, gas therapy has become an emerging treatment. Studies have shown that the proliferation, metastasis and invasiveness of glioma cells exposed to anesthetic gases are obviously inhibited. Therefore, anesthetic gas may play a special therapeutic role in gliomas. In this review, we aim to collect existing research and summarize the rules of using anesthetic gases on glioma, providing potential strategies for further clinical treatment.

Luteolin Exerts Neuroprotection via Modulation of the p62/Keap1/Nrf2 Pathway in Intracerebral Hemorrhage.

Upregulation of neuronal oxidative stress is involved in the progression of secondary brain injury (SBI) following intracerebral hemorrhage (ICH). In this study, we investigated the potential effects and underlying mechanisms of luteolin on ICH-induced SBI. Autologous blood and oxyhemoglobin (OxyHb) were used to establish in vivo and in vitro models of ICH, respectively. Luteolin treatment effectively alleviated brain edema and ameliorated neurobehavioral dysfunction and memory loss in vivo. Also, in vivo, we found that luteolin promoted the activation of the sequestosome 1 (p62)/kelch-like enoyl-coenzyme A hydratase (ECH)-associated protein 1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway by enhancing autophagy and increasing the translocation of Nrf2 to the nucleus. Meanwhile, luteolin inhibited the ubiquitination of Nrf2 and increased the expression levels of downstream antioxidant proteins, such as heme oxygenase-1 (HO-1) and reduced nicotinamide adenine dinucleotide phosphate (NADPH): quinine oxidoreductase 1 (NQO1). This effect of luteolin was also confirmed in vitro, which was reversed by the autophagy inhibitor, chloroquine (CQ). Additionally, we found that luteolin inhibited the production of neuronal mitochondrial superoxides (MitoSOX) and alleviated neuronal mitochondrial injury in vitro, as indicated via tetrachloro-tetraethylbenzimidazol carbocyanine-iodide (JC-1) staining and MitoSOX staining. Taken together, our findings demonstrate that luteolin enhances autophagy and anti-oxidative processes in both in vivo and in vitro models of ICH, and that activation of the p62-Keap1-Nrf2 pathway, is involved in such luteolin-induced neuroprotection. Hence, luteolin may represent a promising candidate for the treatment of ICH-induced SBI.