Significance: Previously, sulfur dioxide (SO2) was recognized as an air pollutant. However, it is found to be endogenously produced in mammalian tissues. As a new gasotransmitter, SO2 is involved in regulating the structure and function of blood vessels, heart, lung, gastrointestinal tract, nervous system, etc.Recent Advances: Increasing evidence showed that endogenous SO2 regulates cardiovascular physiological processes, such as blood pressure control, vasodilation, maintenance of the normal vascular structure, and cardiac negative inotropy. Under pathological conditions including hypertension, atherosclerosis, vascular calcification, aging endothelial dysfunction, myocardial injury, myocardial hypertrophy, diabetic myocardial fibrosis, sepsis-induced cardiac dysfunction, pulmonary hypertension, acute lung injury, colitis, epilepsy-related brain injury, depression and anxiety, and addictive drug reward memory consolidation, endogenous SO2 protects against the pathological changes via different molecular mechanisms and the disturbed SO2/aspartate aminotransferase pathway is likely involved in the mechanisms for the earlier mentioned pathologic processes. Critical Issues: A comprehensive understanding of the biological effects of endogenous SO2 is extremely important for the development of novel SO2 therapy. In this review, we summarized the biological effects, mechanism of action, SO2 detection methods, and its related prodrugs. Future Directions: Further studies should be conducted to understand the effects of endogenous SO2 in various physiological and pathophysiological processes and clarify its underlying mechanisms. More efficient and accurate SO2 detection methods, as well as specific and effective SO2-releasing systems should be designed for the treatment and prevention of clinical related diseases. The translation from SO2 basic medical research to its clinical application is also worthy of further study. Antioxid. Redox Signal. 36, 256-274. 

Sulfur Dioxide: Endogenous Generation, Biological Effects, Detection, and Therapeutic Potential

Significance: Previously, sulfur dioxide (SO2) was recognized as an air pollutant. However, it is found to be endogenously produced in mammalian tissues. As a new gasotransmitter, SO<sub...

Sulfur Dioxide: Endogenous Generation, Biological Effects, Detection, and Therapeutic Potential.

Pulmonary hypertension (PH) is a fatal disease caused by progressive pulmonary vascular remodeling (PVR). Currently, the mechanisms underlying the occurrence and progression of PVR remain unclear, and effective therapeutic approaches to reverse PVR and PH are lacking. Since the beginning of the 21st century, the endogenous sulfur dioxide (SO2)/aspartate transaminase system has emerged as a novel research focus in the fields of PH and PVR. As a gaseous signaling molecule, SO2 metabolism is tightly regulated in the pulmonary vasculature and is associated with the development of PH as it is involved in the regulation of pathological and physiological activities, such as pulmonary vascular cellular inflammation, proliferation and collagen metabolism, to exert a protective effect against PH. In this review, we present an overview of the studies conducted to date that have provided a theoretical basis for the development of SO2-related drug to inhibit or reverse PVR and effectively treat PH-related diseases.

Advances in the research of sulfur dioxide and pulmonary hypertension

Depression and anxiety disorders are prevalent psychiatric conditions, and currently utilized chemical drugs typically come with significant adverse effects. China boasts a wealth of medicinal and food herbs known for their safe and effective properties. 

Network pharmacology screening, in vitro and in vivo evaluation of antianxiety and antidepressant drug-food analogue

Background The pathogenesis of depression is closely related to changes in hippocampal synaptic plasticity; however, the underlying mechanism is still unclear. Brain-specific angiogenesis inhibitor 1-associated protein 2 (BAIAP2), a postsynaptic scaffold protein in excitatory synapses important for synaptic plasticity, is highly expressed in the hippocampus and has been implicated in several psychiatric disorders. However, the role of BAIAP2 in depression remains poorly understood. Methods In the present study, a mouse model of depression was established via exposure to chronic mild stress (CMS). An adeno-associated virus (AAV) vector expressing BAIAP2 was injected into the hippocampal brain region of mice and a BAIAP2 overexpression plasmid was transfected into HT22 cells to upregulate BAIAP2 expression. Depression- and anxiety-like behaviors and dendritic spine density were examined in mice using behavioral tests and Golgi staining, respectively. In vitro, hippocampal HT22 cells were treated with corticosterone (CORT) to simulate the stress state, and the effect of BAIAP2 on CORT-induced cell injury was explored. Reverse transcription-quantitative PCR and western blotting were employed to determine the expression levels of BAIAP2 and those of the synaptic plasticity-related proteins glutamate receptor ionotropic, AMPA 1 (GluA1), and synapsin 1 (SYN1). Results Mice exposed to CMS exhibited depression- and anxiety-like behaviors accompanied by decreased levels of BAIAP2 in the hippocampus. In vitro, the overexpression of BAIAP2 increased the survival rate of CORT-treated HT22 cells and upregulated the expression of GluA1 and SYN1. Consistent with the in vitro data, the AAV-mediated overexpression of BAIAP2 in the hippocampus of mice significantly inhibited CMS-induced depression-like behavior, concomitant with increases in dendritic spine density and the expression of GluA1 and SYN1 in hippocampal regions. Conclusion Our findings indicate that hippocampal BAIAP2 can prevent stress-induced depression-like behavior and may be a promising target for the treatment of depression or other stress-related diseases.

/pdf/hippocampal-baiap2-prevents-chronic-mild-stress-induced-t24r3ryl.pdf

Hippocampal BAIAP2 prevents chronic mild stress-induced depression-like behaviors in mice

Sulfur dioxide derivatives attenuates consolidation of contextual fear memory in mice.

Sulfur dioxide derivatives produce antidepressant- and anxiolytic-like effects in mice

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Sulfur dioxide derivatives attenuates consolidation of contextual fear memory in mice.

Sulfur dioxide derivatives produce antidepressant- and anxiolytic-like effects in mice