ogical diseases.The inhibition of mesangial cell proliferation has become an important therapy for the prevention of glomerular proliferation‑associated diseases. The combined application of immunosuppressants with multiple targets presents a novel direction in the treatment of kidney diseases.  https://www.selleckchem.com/products/bp-1-102.html  The present study was designed to explore the inhibitory effects of tacrolimus (TAC) combined with mycophenolate mofetil (MMF) on the proliferation of mesangial cells based on the cell cycle. In vitro, the levels of the proliferation index markers, Ki67 and cyclin D1, in human mesangial cells (HMCs) were determined by immunofluorescence staining and western blot analysis, respectively. In mice with lupus nephritis (LN), the proliferation of mesangial cells was determined using PAS and Masson's trichrome staining, while immunohistochemistry was used to detect Ki67 and western blot analysis was employed for the evaluation of cyclin D1 levels. The expression of platelet‑derived growth factor (PDGF), a proliferation‑associated protein, was estimated using immunohistochemistry and western blot analysis. In patients with LN, Ki67, cyclin D1 and PDGF expression was estimated by immunohistochemistry. The transforming growth factor‑β1/Smad pathway influenced by TAC and the p38 pathway influenced by MMF were also examined by western blot analysis. The results suggested that the combination of TAC and MMF at half the concentration based on the cell cycle was more effective than monotherapy in inhibiting mesangial cell proliferation in vitro and in vivo. TAC inhibited HMC proliferation by affecting the Smad2 signaling pathway. MMF inhibited HMC proliferation by affecting the p38 signaling pathway. Combined treatment with TAC and MMF significantly improved the clinical indexes of patients with LN without severe adverse effects. On the whole, the findings of the present study validate and reinforce the potential use of the combination of TAC and MMF for the treatment of mesangial proliferative diseases.Psoriasis is an immune‑mediated dermatosis characterized by T‑lymphocyte‑mediated epidermal hyperplasia, for which there are currently no effective clinical treatments. 'Psoriasis 1' is a Chinese herbal medicine formulation that has been recently used extensively in China for treating patients with psoriasis. However, the molecular mechanism of action of this potent formulation has not yet been fully elucidated. In the present study, the effects of 'Psoriasis 1' on T ymphocytes in patients with psoriasis were investigated and the underlying molecular mechanism was discussed. Blood samples were collected from 40 patients with psoriasis. ELISA was employed to assess the levels of tumour necrosis factor‑α, interferon‑γ, interleukin (IL)‑2, IL‑6, transforming growth factor‑β, IL‑4, IL‑12, IL‑23 and vitamin D (VD). Western blot and quantitative PCR analyses were used to investigate the expression levels of VD receptor (VDR) and signal transducer and activator of transcription (STAT)4 in T lymphocytes. 'Psoriasis 1' was observed to significantly increase CD4+ T cells. It also notably upregulated the mRNA and protein expression of VDR, and downregulated the mRNA and protein expression of STAT4. Moreover, the suppression of VDR was found to aggravate the inflammatory response, which was reversed by 'Psoriasis 1.' Thus, this formulation reportedly decreased the inflammation mediated by T lymphocytes in patients with psoriasis through inhibiting VDR‑mediated STAT4 inactivation.Thymosin‑β 4 (Tβ4) has been reported to exert a pro‑angogenic effect on endothelial cells. However, little is known on the role and underlying mechanisms of Tβ4 on critical limb ischemia (CLI). The present study aimed therefore to investigate the mechanisms and pro‑angiogenic effects of Tβ4 in CLI mice. Tβ4 overexpression lentiviral vector was first transfected into HUVEC and CLI mice model, and inhibitors of Notch pathway (DAPT) and NF‑κB pathway (BMS) were also applied to HUVEC and CLI mice. Subsequently, MTT, tube formation and wound healing assays were used to determine the cell viability, angiogenesis and migratory ablity of HUVEC, respectively. Western blotting, reverse transcription, quantitative PCR, immunofluorescence and immunohistochemistry were used to detect the expression of the angiogenesis‑related factors angiopoietin‑2 (Ang2), TEK receptor tyrosine kinase 2 (tie2), vascular endothelial growth factor A (VEGFA), CD31 and α‑smooth muscle actin (α‑SMA) and the Notch/NF‑κB pathways‑related factors NOTCH1 intracellular domain (N1ICD), Notch receptor 3 (Notch3), NF‑κB and p65 in HUVEC or CLI mice muscle tissues. The results demonstrated that Tβ4 not only enhanced the cell viability, angiogenesis and migratory ability of HUVEC but also promoted the expression of Ang2, tie2, VEGFA, N1ICD, Notch3, NF‑κB, and phosphorylated (p)‑p65 in HUVEC. In addition, Tβ4 promoted the expression of CD31, α‑SMA Ang2, tie2, VEGFA, N1ICD and p‑p65 in CLI mice muscle tissues. Treatment with DAPT and BMS had opposite effects of Tβ4, whereas Tβ4 reversed the effect of DAPT and BMS. The findings from the present study suggested that Tβ4 may promote angiogenesis in CLI mice via regulation of Notch/NF‑κB pathways.Vascular endothelial cell apoptosis is regulated by microRNA‑133a (miR‑133a), which participates in the formation of atherosclerotic (AS) plaques, leading to the development of several cardiovascular diseases. Salidroside (SAL), the main component of Rhodiola, is considered to exert anti‑AS effect; however, its mode of action remains unclear. Thus, the present study aimed to determine whether SAL inhibits endothelial cell apoptosis through the miR‑133a pathway. Cultured human coronary artery endothelial cells (HCAECs) were exposed to oxidized low‑density lipoprotein (ox‑LDL). Cell viability and cytotoxicity were monitored by MTT assay. In parallel, the mRNA expression levels of miR‑133a and Bcl‑xL, and the protein levels of anti‑apoptotic Bcl‑xL and activated caspase‑3 were measured. The apoptotic levels were examined by flow cytometry. Furthermore, the effects of silencing and overexpressing miR‑133a on the parameters mentioned above were evaluated. Exposure to ox‑LDL induced an increase in the expression of miR‑133a, with a concomitant decrease in the level of Bcl‑xL in the HCAECs; these effects were reversed by treatment with SAL.