This review supports the hypothesis that the regulation of GJCs between astrocytes could be an underlying mechanism for the therapeutic effect of antidepressants.

Major depressive disorder (MDD) is a leading chronic mental illness worldwide, characterized by anhedonia, pessimism and even suicidal thoughts. Connexin 43 (Cx43), mainly distributed in astrocytes of the brain, is by far the most widely and ubiquitously expressed connexin in almost all vital organs. Cx43 forms gap junction channels in the brain, which mediate energy exchange and effectively maintain physiological homeostasis. Increasing evidence suggests the crucial role of Cx43 in the pathogenesis of MDD. Neuroinflammation is one of the most common pathological features of the central nervous system dysfunctions. Inflammatory factors are abnormally elevated in patients with depression and are closely related to nearly all links of depression. After activating the inflammatory pathway in the brain, the release and uptake of glutamate and adenosine triphosphate, through Cx43 in the synaptic cleft, would be affected. In this review, we have summarized the association between Cx43 and neuroinflammation, the cornerstones linking inflammation and depression, and Cx43 abnormalities in depression. We also discuss the significant association of Cx43 in inflammation and depression, which will help to explore new antidepressant drug targets.

Ginsenoside Rg1, a traditional Chinese medicine monomer, has been shown to have antidepressant effects. We previously found that Rg1 exerts antidepressant effects by improving the gap junction channels (GJCs) dysfunction; however, the downstream mechanisms through which Rg1 ameliorates GJC dysfunction remain unclear. Since hemichannels directly release glutamate, GJC dysfunction decreases the expression levels of glutamate transporters in astrocytes, and glutamatergic system dysfunction plays an essential role in the pathogenesis of depression. The glutamatergic system may be a potential downstream target of Rg1 that exerts antidepressant effects. Therefore, in this study, we aimed to determine the downstream mechanisms by which Rg1 ameliorated GJC dysfunction and exerted its antidepressant effects. Corticosterone (CORT) is used to mimic high glucocorticoid levels in patients with depression in vitro. Primary cortical astrocytes were isolated and phosphorylation of connexin43 (Cx43) as well as the functions of hemichannels, GJCs, and the glutamatergic system were evaluated after drug treatment. Rg1 pretreatment reversed the anomalous activation of Cx43 phosphorylation as well as the dysfunction of hemichannels, GJCs, and the glutamatergic system induced by CORT. These results suggest that Rg1 can ameliorate CORT-induced dysfunction of the glutamatergic system in astrocytes by potentially reducing Cx43 phosphorylation and inhibiting opening of hemichannels, thereby improving GJC dysfunction.

The lignin present in lignocellulose seriously affects the efficiency of cellulose enzymatic hydrolysis. In addition, lignin adsorbs high-cost cellulase, causing greater economic losses. Lignin can also disturb the site of action of cellulase and reduce the efficiency of hydrolysis. Therefore, if lignin is removed or surface modified before cellulose enzymatic hydrolysis, the enzymatic hydrolysis efficiency of lignocellulosic biomass will be greatly improved. In this paper, the cellulose enzymatic properties of bamboo biomass being treated with dilute acid and alkaline under the intervention of biosurfactant rhamnolipid were evaluated. The effects of rhamnolipids on the adsorption characterization of cellulose on pretreated bamboo were studied. Besides, the inter-communication between rhamnolipids and cellulose was investigated by fluorescence probe. The results showed that rhamnolipids could have a positive effect on the enzymatic hydrolysis of bamboo biomass by reducing the non-productive adsorption of cellulase on the surface of lignocellulose. The outcome illustrated that cellulase could be combined with rhamnolipids micelles, participating in the formation of rhamnolipids micelles, thereby increasing the internal hydrophobicity of the micelles, but could not change the properties of rhamnolipids micelles higher than one CMC (Critical Micelle Concentration). It can be seen that the interaction between rhamnolipids and cellulase is beneficial to enhance the stability and enzymatic activity of cellulase, thereby improving the enzymatic hydrolysis efficiency of cellulose in biomass. Based on these results, a theoretical knowledge about the mechanism of enhancing the enzymatic hydrolysis efficiency of lignocellulose by biosurfactants rhamnolipids is provided.