Glehniae Radix has a wide range of pharmaceutical applications, and research on its main components has mainly focused on coumarins, alkaloids, lignans, and flavonoids, while neglecting the research on polysaccharides. Literature reports and our previous studies have shown that polysaccharides have certain therapeutic significance in immune regulation, antioxidant, anti-inflammatory and other aspects. Herein, the rat model of ulcerative colitis (UC) was established to evaluate the anti-inflammatory efficacy of the prepared Glehniae Radix polysaccharide (GLP) from the perspectives of inflammatory factors, intestinal tissue morphology, and microflora changes. The polysaccharides are mainly composed of galacturonic acid, rhamnose, glucose, galactose, and arabinose in molar ratios of 1.4:9.2:33.3:2.5:2.9, and GLP could downregulate the expression pro-inflammatory factors (interleukin-6, tumor necrosis factor-α, and interferon-γ) and significantly upregulate the expression of anti-inflammatory factor (interleukin-10). In addition, Glehniae Radix aqueous extract (GLA), GLP with low dosage (GLPL) and GLP with high dosage (GLPH) could increase the number of goblet cells, enhance the integrity of crypt structure, and reverse the status of inflammatory infiltrating cells. Moreover, GLA and GLPH could upregulate Lactobacillus and Lachnoclostridium in UC rats, and appropriately downregulate Lachnospiraceae_NK4A136_group, thereby optimizing the proportion of bacterial flora and improving the intestinal microbial environment. Our findings not only be valuable as theoretical materials for the further clinical applications of GLP, but the identified biomarkers and metabolic pathways also provide new clues for the diagnosis of UC.


Inflammatory stimulation plays a significant role in the development and worsening of insulin-resistant diabetes. Therefore, it is crucial to identify therapeutic agents that can alleviate insulin resistance by targeting inflammation. Here, we present evidence that Bakuchiol (BL), a monoterpene phenolic compound first discovered from Psoralea corylifolia L. as traditional Chinese medicine, can effectively improve insulin resistance in diabetic mice through anti-inflammation. Our findings demonstrate that BL alleviates inflammation by inhibiting the toll-like receptor 4/nuclear factor κB/mitogen-activated protein kinase axis, consequently enhancing insulin receptor signaling through the c-Jun N-terminal kinase/suppressors of cytokine signaling 3/insulin receptor substrate1 pathway and improving glucolipid homeostasis. Furthermore, the insulin recovery achieved with BL (60 mg/kg) was comparable to that of metformin (200 mg/kg). These results provide further support for considering BL as a potential treatment option for insulin-resistant diabetes mellitus.

Inflammation caused by obesity, particularly in adipose tissue and the liver, can lead to insulin resistance (IR) and trigger type 2 diabetes (T2DM). It is crucial to identify therapeutic agents that alleviate IR by reducing inflammation. Here, we report that isobavachromene (IB), a flavonoid derived from Psoralea corylifolia Linn., ameliorates IR in 3T3-L1 adipocytes by inhibiting the MAPK/NF-κB signaling pathway. We first found that IB could promote glucose uptake in 3T3-L1 adipocytes by activating the PI-3K/Akt signaling pathway and was more effective than the positive control sodium orthovanadate at concentrations ranging from 25 to 100 μmol/L. Additionally, IB inhibited RAW264.7 macrophage infiltration into 3T3-L1 adipocytes and suppressed the secretion of inflammatory factors from RAW264.7 macrophages, as well as the phosphorylation levels of key proteins (NF-κB P65, ERK1/2, JNK, and P38) in the NF-κB and MAPK signaling pathways. In summary, IB improves glucose uptake in IR adipocytes, activates the PI-3K/Akt signaling pathway, inhibits the JNK and NF-κB inflammatory signaling pathways, and reduces adipocyte inflammation, thereby improving of IR in 3T3-L1 adipocytes.
