To investigate the efficacy and mechanism of the Qingre Huayu Fang () on atherosclerotic vulnerable plaque in apolipoprotein E (ApoE) knockout mice through the ubiquitin proteasome pathway. Sixty 8-week-old C57BL/6J ApoE knockout mice were fed a high-fat for 12 weeks and randomly divided into four treatment groups (n = 15 each) high-fat control, bortezomib (a proteasome inhibitor), bortezomib combined with Qingre Huayu Fang, and Qingre Huayu Fang alone. Aortic sections were examined for plaque development, inflammatory cell infiltration, type Ⅰ/Ⅲ collagen expression and immunohistochemical staining of CD40L, nuclear factor-kappa B (NF-κB)/P65 and ubiquitin. Mice in the high-fat control group had obvious atherosclerosis, with increased aortic plaque area. The degree of atherosclerosis of the atherosclerotic plaque was reduced in all of the treatment groups that received bortezomib and/or Duzhong (Cortex Eucommiae) Qingre Huayu. The expression of NF-?B, CD40L and ubiquitin were all reduced in the group that received combination bortezomib + Qingre Huayu Fang. The Qingre Huayu Fang inhibited aortic atherosclerosis in mice through a mechanism that may involve inhibition of the ubiquitin proteasome pathway.The Qingre Huayu Fang inhibited aortic atherosclerosis in mice through a mechanism that may involve inhibition of the ubiquitin proteasome pathway. To investigate the efficacy of the full composition granules of Huanglian (Rhizoma Coptidis) (FGC) on the serum monocyte chemotactic protein-1 (MCP-1) and connective tissue growth factor (CTGF) levels and kidney nuclear factor-κB (NF-κB) expression in rats with high-fat diet-induced diabetes. Diabetes was induced in rats by feeding a high-fat chow combined with intravenous streptozotocin injection. Forty diabetic Sprague- Dawley rats were randomly assigned to a normal group (NG), model group (MG), irbesartan group (IG), and low-, middle-, and high-dosage FGC groups (LFGC, MFGC, HFGC), with eight rats per group. The IG rats received 31.25 mg·kg－1·d－1 irbesartan tablets, whereas those in the LFGC, MFGC, and HFGC were administered 52, 312.5, and 625 mg·kg－1·d－1 FGC, respectively. After 12 weeks, bodyweight (BW), left kidney weight (KW), hemoglobin A1c (HbA1c), serum creatinine (Scre), blood urea nitrogen (BUN), and serum MCP-1 and CTGF levels were determined, pathological changes of the kidney were recorded,hropathy in rats with high-fat diet-induced diabetes.FGC may alleviate potential kidney injury by decreasing the serum MCP-1 and CTGF levels and inhibiting NF-kB expression in diabetic nephropathy in rats with high-fat diet-induced diabetes. To investigate how compound Sophorae decoction (CSD) works on rats' models of ulcerative colitis (UC) induced by 2,4,6-trinitrobenzenesulfonic acid solution (TNBS) by metabolomics studies of colon, liver, and kidney tissue extracts. Rats with UC induced by TNBS enema were used as models in this study. Metabolic profiles of the three tissues were analyzed and pathway analysis of biomarkers was performed after CSD administration and further integration of metabolic networks. Thirteen biomarkers were screened from colon, liver, and kidney tissue extracts, and the levels of these substances were up- or down-regulated in the model group, but their levels were reversed after CSD administration. These biomarkers were mainly related to Phenylalanine, tyrosine and tryptophan biosynthesis, Phenylalanine metabolism, Glutathione metabolism, Arachidonic acid metabolism, Nicotinate and nicotinamide metabolism, Alanine, aspartate and glutamate metabolism. CSD could significantly ameliorate the symptoms of UC by regulating multiple metabolic pathways.CSD could significantly ameliorate the symptoms of UC by regulating multiple metabolic pathways. To investigate the effects of Gyejibokryeong-Hwan (Guizhifuling-wan, GBH) on muscle injury in a mouse model of muscle contusion. C57/BL6 mouse biceps femoris muscles were injured using the drop-mass method and injured animals were treated orally with GBH (50, 100, or 500 mg/kg) once a day for 7 d. Open field and treadmill running tests were performed to assess functional recovery from muscle injury. The production of pro-inflammatory cytokines was examined by enzyme-linked immunosorbent assay and Western blotting analysis. Expression of the muscle regeneration biomarkers, myoblast determination (MyoD), myogenic factor 5 (Myf5), and smooth muscle actin (α-SMA), in the biceps femoris muscle was investigated at the protein and mRNA level by Western blotting and real time-PCR, respectively. Histological analysis was performed using hematoxylin and eosin staining. Finally, myosin heavy chain production was investigated in differentiated C2C12 myoblasts in the presence of GBH. GBH treatment markedly improved locomotion and running behavior. GBH significantly inhibited the secretion of monocyte chemoattractant protein-1 into the bloodstream in muscle-contused animals. The levels of MyoD, Myf5, and α-SMA protein and mRNA were significantly up-regulated by GBH in injured muscle tissue. Histological studies suggested that GBH facilitated recovery from muscle damage. However, GBH did not induce the production of myosin heavy chain in vitro. Overall, the present study suggested that GBH improves the recovery of the injured muscles in the mouse model of muscle contusion.Overall, the present study suggested that GBH improves the recovery of the injured muscles in the mouse model of muscle contusion. To investigate whether Hydrolyzed Seawater Pearl tablet (HSPT) could modulate the Th1/Th2 imbalance in an immunosuppressed mouse model with Th1 to Th2 shift induced by Cyclosporine A (CsA) which can be used in the clinical treatment of Th2 to Th1 shift diseases, and explore the possible mechanism for the adjuvant therapeutic efficacy of HSPT on recurrent respiratory infections (RRI) and acquired immune deficiency syndrome (AIDS). The mice were randomly divided into six groups of five animals each, namely normal group, model group, lentinan polysaccharide tablet (LPT) group and three HPST treated groups. HPST treated groups were administered with HPST (0.51, 1.02, 2.04 g/kg) via intragastric gavage (i.g) for 30 consecutive days. buy TVB-3166 LPT used as reference drug for positive control, LPT group was administered with LPT (8.2 mg/kg) for 30 consecutive days. Normal group and model group were received distilled water. The animals in model group, LPT group and HPST treated groups were injected intraperitoneally with CsA (50 mg/kg) to establish the immunosuppressed mice model with Th1 to Th2 shift on the 20th, 22nd and 24th day, one hour after the administration of the respective treatment.