Objective:To investigate the expression and clinical significance of microRNA-30a in renal cell carcinoma (RCC). Methods:The miRNA-30a expression in renal tissues and cell lines was detected using quantitative real-time polymerase chain reac-tion (qRT-PCR), and the relationship between miRNA-30a expression and the clinicopathological features of RCC was analyzed. The effect of miRNA-30a on cancer cells was evaluated using methyl thiazolyl tetrazolium (MTT) assay. In addition, a bioinformatics algo-rithm was adopted to predict the potential targets of miRNA-30a. Results:miRNA-30a was downregulated both in RCC tissues and cell lines. Patients with higher miRNA-30a expression exhibited better prognosis than those with lower miRNA-30a expression. Bioin-formatics algorithm and qRT-PCR both indicated that metadherin (MTDH) was a target of miRNA-30a. Moreover, MTT results showed that miRNA-30a could inhibit cell proliferation. Conclusion:miRNA-30a was inhibited in renal cancer, and low miRNA-30a expres-sion was associated with poor prognosis. In addition, miRNA-30a could inhibit the growth of cells through MTDH.

Objective: To study the effects of TCFC on proliferation and osteogenic action of osteoblast in neonatal rat calvaria cultures in vitro. Methods: Osteoblasts were isolated from neonatal rat calvaria through trypsin and collagenase digestion. The proliferation and collagen synthesis were assayed by 3H TdR and 3H proline incorporation. The activity of ALP was measured by p nitrophenyl sodium phosphate assay. The ipriflavone was used as positive control drug.Results: TCFC significantly promoted bone cell proliferation, alkaline phosphatase activity and collage synthesis.Conclusion: TCFC had the anti osteoporosis action by promoting osteoblast proliferation, ALP activity and collage synthesis.

The Philippines’ medical system is mainly based on the provincial responsibility system and the limited hierarchical. The Philippine government implement Philhealth program which can provide medical insurance for most people. The top 10 fatal diseases in this country includes ischemic heart disease, stroke, lower respiratory tract infection and so on. Of these diseases, the increasing rate of hypertensive heart disease, chronic kidney disease and diabetes are fast. Bone setting, massage and herbal medicine are the major form of traditional medicine in the Philippines. The acceptance of acupuncture and moxibustion by the government and local people is relatively high acupuncture and moxibustion therapy has been included in its medical insurance. There are many limitations on the development of Traditional Chinese Medicine (TCM) theory and Chinese herbal medicine in the Philippines, and the clinical application of acupuncture and Chinese herbal medicine is still limited. TCM education in the Philippines is still not systematic. Therefore, it is suggested to improve the education system of TCM, strengthen the promotion of acupuncture and moxibustion, give full play of the advantages of TCM for native high-risk diseases, and to make use of modern technologies such as telemedicine.

ObjectiveTo explore the effects of Kaixuan Jiedu core prescription （KXJD） on sphingolipid metabolism in the mouse model of imiquimod-induced psoriasis-like skin lesions. MethodsThirty-seven male C57BL/6J mice were randomly assigned into five groups： healthy control （n=11）， model （n=11）， methotrexate （MTX， n=5）， low-dose （15.21 g·kg^-1） KXJD （n=5）， and high-dose （30.42 g·kg^-1） KXJD （n=5）. Psoriasis-like skin lesions were induced in mice with 62.5 mg 5% imiquimod cream applied on the back. The KXJD groups and MTX group were treated with 0.2 mL corresponding decoction and MTX， respectively， by gavage daily， while the other groups were given an equal volume of normal saline by the same way. After 5 days of treatment， back skin lesions were collected. Firstly， healthy control and model mice were selected for tandem mass tag （TMT） quantitative proteomics （control vs model=3 vs 3） and targeted lipid metabolomics （control vs model=11 vs 11）. Then， the binding degree between core components and target proteins was predicted via network pharmacology and molecular docking. Finally， an animal experiment was performed to decipher the specific regulation mechanism of KXJD on sphingolipid metabolism. Immunohistochemistry was employed to determine the expression level of sphingosine-1-phosphate （S1P）， and Western blot was employed to determine the expression levels of sphingosine kinase 2 （SPHK2） and monocyte chemotactic protein-1 （MCP-1）. ResultsTMT proteomics and targeted lipid metabolomics suggested that sphingolipid metabolism was active in the psoriatic skin， and key proteases ［serine palmitoyltransferase， long chain base subunit 2 （SPTLC2）， SPHK2， delta（4）-desaturase sphingolipid 1 （Degs1）， and ceramide synthase 4 （CerS4）］ and 8 sphingolipid metabolites （including ceramides， sphingol， sphingomyelin， and glycosphingolipid） expressed abnormally （P<0.05） compared with those in the healthy skin. The molecular docking results indicated that the binding energy between the active components （quercetin， kaempferol， and luteolin） in KXJD and key proteins involved in sphingolipid metabolism was less than-8 kal·mol^-1. Further experimental verification showed elevated expression levels of SPHK2， S1P， and MCP-1 in psoriatic skin compared with healthy skin （P<0.05）， and KXJD down-regulated the expression levels of SPHK2， S1P， and MCP-1 compared with the model group （P<0.05）. ConclusionThis study indicates that there is an imbalance in sphingolipid metabolism in psoriatic skin lesions. KXJD may reduce psoriasis-like lesions in mice by regulating sphingolipid metabolism via the SPHK2/S1P/MCP-1 pathway.

ObjectiveTo explore the effects of Kaixuan Jiedu core prescription （KXJD） on sphingolipid metabolism in the mouse model of imiquimod-induced psoriasis-like skin lesions. MethodsThirty-seven male C57BL/6J mice were randomly assigned into five groups： healthy control （n=11）， model （n=11）， methotrexate （MTX， n=5）， low-dose （15.21 g·kg^-1） KXJD （n=5）， and high-dose （30.42 g·kg^-1） KXJD （n=5）. Psoriasis-like skin lesions were induced in mice with 62.5 mg 5% imiquimod cream applied on the back. The KXJD groups and MTX group were treated with 0.2 mL corresponding decoction and MTX， respectively， by gavage daily， while the other groups were given an equal volume of normal saline by the same way. After 5 days of treatment， back skin lesions were collected. Firstly， healthy control and model mice were selected for tandem mass tag （TMT） quantitative proteomics （control vs model=3 vs 3） and targeted lipid metabolomics （control vs model=11 vs 11）. Then， the binding degree between core components and target proteins was predicted via network pharmacology and molecular docking. Finally， an animal experiment was performed to decipher the specific regulation mechanism of KXJD on sphingolipid metabolism. Immunohistochemistry was employed to determine the expression level of sphingosine-1-phosphate （S1P）， and Western blot was employed to determine the expression levels of sphingosine kinase 2 （SPHK2） and monocyte chemotactic protein-1 （MCP-1）. ResultsTMT proteomics and targeted lipid metabolomics suggested that sphingolipid metabolism was active in the psoriatic skin， and key proteases ［serine palmitoyltransferase， long chain base subunit 2 （SPTLC2）， SPHK2， delta（4）-desaturase sphingolipid 1 （Degs1）， and ceramide synthase 4 （CerS4）］ and 8 sphingolipid metabolites （including ceramides， sphingol， sphingomyelin， and glycosphingolipid） expressed abnormally （P<0.05） compared with those in the healthy skin. The molecular docking results indicated that the binding energy between the active components （quercetin， kaempferol， and luteolin） in KXJD and key proteins involved in sphingolipid metabolism was less than-8 kal·mol^-1. Further experimental verification showed elevated expression levels of SPHK2， S1P， and MCP-1 in psoriatic skin compared with healthy skin （P<0.05）， and KXJD down-regulated the expression levels of SPHK2， S1P， and MCP-1 compared with the model group （P<0.05）. ConclusionThis study indicates that there is an imbalance in sphingolipid metabolism in psoriatic skin lesions. KXJD may reduce psoriasis-like lesions in mice by regulating sphingolipid metabolism via the SPHK2/S1P/MCP-1 pathway.