Atherosclerosis (AS) is a chronic inflammatory disease resulting from lipid metabolism disorders and immune imbalances. Dendritic cells (DCs) are key cells that regulate adaptive and adaptive immunity. When DCs engulf excessive amounts lipids, their function is altered, thereby, accelerating the inflammatory process of AS. Cellular lipophagy serves to reduce lipid accumulation and maintain cellular lipid metabolism balance. In this study, we investigated the effectiveness of 2,3,5,4'-tetrahydroxystilbene 2-O-β-D-glucoside (TSG) in intervening in the promotion of DCs lipid accumulation by ox-LDL, as well as its role in downregulating lipophagy. Our findings indicate that TSG reduces the maturity of DCs and promotes the differentiation of T cells towards Treg, thereby correcting the imbalanced Treg/Th17. These effects of TSG are closely associated with its inhibition of the PI3K-AKT-mTOR signaling pathway. After administering TSG to ApoE-/- mice that were fed a high-fat diet, there was a noticeable decrease in harmful blood lipids found in the serum. Additionally, the imbalanced Treg/Th17 levels in the spleen were restored, and the levels of pro-inflammatory factor IL-6 and IL-17A in the serum decreased, while the level of anti-inflammatory factor IL-10 increased. Furthermore, the arterial DCs showed a decrease in P62 content. Ultimately, these changes resulted in a reduction in plaque area. It is worth noting that the autophagy inhibitor chloroquine significantly altered the effects of TSG on ApoE-/- mice. In conclusion, this study reveals that TSG can alleviate AS. This is partly achieved through the activation of autophagy in DCs. By intervening in the lipophagy of DCs, it is possible to regulate the immune function of these cells, which in turn helps control the inflammation associated with AS. This presents a potential method for intervening in AS.

Cholesterol aggregation in dendritic cells (DCs) triggers an inflammatory response and accelerates the development of atherosclerosis (AS). Resveratrol (RES), a natural compound with anti-inflammatory and cholesterol metabolism regulatory properties, has been shown to influence the maturation and inflammatory functions of DCs. However, its relationship with cholesterol metabolism remains unclear. This study aimed to explore the roles of RES in cholesterol metabolism and inflammatory behaviors of DCs in the context of AS. We analyzed the effect of RES on cholesterol efflux from ApoE−/− bone marrow-derived dendritic cells (BMDCs) using qRT-PCR, Western blot, and cholesterol efflux assays; identified the inflammatory status of RES-treated BMDCs and co-cultured T cells using flow cytometry and ELISA; confirmed the effect of RES on blood lipids, atherosclerotic lesions, cholesterol metabolism, and inflammatory response in high-fat diet and lipopolysaccharide-treated ApoE−/− mice; and explored the potential targets of RES in regulating inflammatory behavior via molecular docking. The results revealed that RES promotes cholesterol efflux, increases the expression of efflux transporter ABCA1, and decreases liver X receptor alpha (LXRα) expression in response to a decrease in intracellular cholesterol in ApoE−/− BMDCs. RES also reduced MHC-II+ cells and downregulated costimulatory molecule CD80 in BMDCs with decreased IL-6 and increased IL-2 production, and suppressed T-cell activation and modulates IL-22 and IL-10 secretion via BMDCs. Furthermore, we confirmed that RES relieves arterial lesions and regulates blood lipids in ApoE−/− mice. RES demonstrated ABCA1 upregulation and LXRα downregulation effects in the aorta and regulated costimulation molecules and Th17/Treg cytokines in the spleen. Furthermore, RES showed multiple hydrogen bonding and low binding energy with ABCA1, suggesting that ABCA1 is a potential target of RES to modulate the inflammatory properties of BMDCs. Our study demonstrated that RES regulates cholesterol efflux and inflammatory behavior in BMDCs, contributing to the control of AS progression and offering new insights for managing inflammatory diseases.

Background Atherosclerosis (AS), which characterized with the accumulation of lipids on the vessel wall, is the pathological basis of many cardiovascular diseases (CVD) and seriously threatens human health. Resveratrol (RES) has been reported to be benefit for AS treatment. This research aimed to observe the effects of RES on AS induced by high-fat diet (HFD) and LPS in ApoE −/− mice and investigate the underlying mechanism. Methods ApoE −/− mice were fed with HFD companied with LPS to induce AS and RES was administrated for 20 weeks. Splenic CD4 + T cells were cultured and treated with anti-CD3/CD28 together with LPS, and RES was added. Serum lipids and the atherosclerotic areas of aortas were detected. The activation of CD4 + T cells were investigated both in vivo and in vitro and the expression of DNA methyltransferases (Dnmt) in CD4 + T cells were measured. Results In vivo, administration of RES prevented HFD and LPS induced dysfunction of serum lipids including TC (total cholesterol), TG (triglyceride), LDL-C (low density lipoprotein cholesterol) and HDL-C (high density lipoprotein cholesterol), ameliorated the thickened coronary artery wall and decreased the areas of atherosclerotic lesion on aortas. Besides, RES decreased the number of CD4 + T cells in peripheral blood, decreased the expression of CD25 and CD44, but not affected the expression of L-selectin (CD62L). In vitro, RES decreased the expression of Ki67, CD25 and CD44 in CD4 + T cells. Moreover, RES increased the secretion of IL-2, IL-10 and TGF-β1, decreased IL-6. In addition, RES decreased both the mRNA and protein level of Dnmt1 and Dnmt3b in CD4 + T cells. Conclusion These results indicated that RES ameliorated AS induced by HFD companied with LPS in ApoE −/− mice, inhibited the proliferation and activation of CD4 + T cells and regulated the expression of Dnmt1 and Dnmt3b.

The aim of this study was to determine the inhibitory action of alantolactone, a gradient of traditional Chinese medicine Inulae Radix (Tu-Mu-Xiang), on herpes simplex virus 1 (HSV-1). African green monkey kidney cells (Vero cells) were infected with HSV-1 and the protective effects of alantolactone on Vero cells were examined. At concentrations of 10-6, 10-7, and 10-8 g/mL, alantolactone did not have a marked harmful effect on the viability of Vero cells according to an MTT assay. Based on the cytopathic effect (CPE) and MTT assays, alantolactone at these concentrations exhibited antiviral action and protected cells from being damaged by HSV-1. Results indicated that alantolactone had potent anti-HSV-1 action and provided evidence for use of Inulae Radix in the treatment of HSV-1 infection.

Endometriosis is a common disease in females of reproductive age and has the classic characteristic of mononuclear cell infiltration into lesions. Shikonin is an anti-inflammatory phytocompound obtained from Lithospermum erythrorhizon whose potential therapeutic effects in the treatment of endometriosis remain unclear. The working hypothesis of the present study was that shikonin is capable of inhibiting the development of endometriosis by inhibiting the chemotactic effect. In a murine model of endometriosis, shikonin significantly inhibited the growth of human endometrial tissue implanted into severe combined immunodeficiency (SCID) mice (P<0.05) and no adverse effects were observed. Mouse regulated upon activation normal T-cell expressed and secreted (mRANTES) levels in the peritoneal fluid of the animal endometriosis model were higher than those in normal SCID mice (P<0.05) and decreased significantly following shikonin treatment in a dose-dependent manner (P<0.05). Peritoneal fluid from SCID mice treated with shikonin inhibited the chemotaxis of monocytes; this inhibitory effect was eradicated by mRANTES antibody. In vitro, shikonin significantly inhibited RANTES expression in U937 cells that were cultured alone or co-cultured with human mesothelial and endometrial stromal cells. In addition, shikonin inhibited the RANTES-induced chemotaxis of U937 cells (P<0.05). The results indicate that shikonin inhibits the development of endometriosis by various mechanisms, including the inhibition of RANTES expression and the reduction of mononuclear cell migration to lesions. Therefore, shikonin may be a novel, useful and safe agent for treating endometriosis.

Aim: To observe the pharmacological actions of Mailuoning sodium chloride injection against cerebral ischemia. Method: The electric coagulation method was used to establish rat middle cerebral artery occlusion model. Rat middle cerebral artery postischemic reperfusion model was made by means of cotton thread insertion method. The mouse acute incomplete cerebral ischemia was observed by ligation method. In situ experiment of dogs was employed to assess the influences of agents on cerebral circulation. Result: The agent had the protective effects against experimental cerebral ischemia in the above-mentioned three animal models. The content of malondialdehyde decreased and the activity of superoxide dismutase increased by the agent.The agent could also decrease the cerebral vessel resistance and increase the cerebral blood flow in anesthetic dogs. Conclusion: The agent could improve the cerebral ischemia in experimental animals, which might be associated with its cerebral vessal relaxation and anti-lipid peroxidation mediated by free radicals.