Advances in Experimental and Clinical Research of the Gouty Arthritis Treatment with Traditional Chinese Medicine.

Gouty arthritis (GA) is a multifactorial disease whose pathogenesis is utterly complex, and the current clinical treatment methods cannot wholly prevent GA development. Western medicine is the primary treatment strategy for gouty arthritis, but it owns an unfavorable prognosis. Therefore, the prevention and treatment of GA are essential. In China, traditional Chinese medicine (TCM) has been adopted for GA prevention and treatment for thousands of years. Gout patients are usually treated with TCM according to their different conditions, and long-term results can be achieved by improving their physical condition. And TCM has been proved to be an effective method to treat gout in modern China. Nevertheless, the pharmacological mechanism of TCM for gout is still unclear, which limits its spread. The theory of prevention and treatment of gout with TCM is more well acknowledged in China than in abroad. In this article, Chinese herbs and ancient formula for gout were summarized first. A total of more than 570 studies published from 2004 to June 2021 in PubMed, Medline, CNKI, VIP, Web of Science databases and Chinese Pharmacopoeia and traditional Chinese books were searched; the current status of TCM in the treatment of GA was summarized from the following aspects: articular chondrocyte apoptosis inhibition, antioxidative stress response, inflammatory cytokine levels regulation, uric acid excretion promotion, immune function regulation, uric acid reduction, and intestinal flora improvement in subjects with gout. The literature review concluded that TCM has a specific curative effect on the prevention and treatment of GA, particularly when combined with modern medical approaches. However, lacking a uniform definition of GA syndrome differentiation and the support of evidence-based medicine in clinical practice have provoked considerable concern in previous studies, which needs to be addressed in future research.

Granulocyte-macrophage colony-stimulating factor and interleukin 4 induce the malignant transformation of the bone marrow-derived human adult mesenchymal stem cells.

BACKGROUND: The purpose of the study was to examine the effects of granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin 4 (IL-4) on the bone-marrow-derived human adult mesenchymal stem cells (hMSCs). METHODS: The hMSCs were isolated and cultured with GM-CSF and IL-4 for a period of one month. A single colony of transformed cells was then isolated and their phenotype was characterized by morphology, surface marker expression, and in vivo tumorigenesis. RESULTS: After one month culture, the transformed mesenchymal cells exhibited the morphology and phenotype similar to those of tumor cells, and also caused multiple fast growing lung deposits when it was injected into immunodeficient mice. CONCLUSION: Cytokines-driven malignant transformation of hMSCs may be a useful model for studying signaling pathways initiating malignant transformation of hMSC.

[Progresses in bone tissue engineering].

Bone tissure engineering plays an important role in tissure engineering. It typically uses an osteoblasts, artificial extracellular matrix (scaffold), and osteoinductive factors which promote cell attachment, differentiation, and mineralized bone formation. So it contents three problems at least: osteoblasts culture in vivo and in vitro, scaffold studies and regulation factors. Bone defect caused by trauma, tumor and inflammation is a frequent and formidable problem in clinical orthopedics. It appears that artificial bone produced by bone tissure engineering can save the problem well. With the development of tissue engineering, bone tissue engineering is developing rapidly. However, seldom experiments are on human body, and fewer productions of bone tissure engineering are used in clinic.

[Osteoblastic differentiation and in vivo osteogenic activity of marrow-derived mesenchymal stem cells stimulated by Tacrolimus: experiment with rats].

OBJECTIVE: To investigate the effect of the immunosuppressant Tacrolimus (FK506) on the osteoblastic differentiation and in vivo osteogenic inducement of bone marrow-derived mesenchymal stem cells (MSCs). METHODS: MSCs were derived from Fischer 344 rats. Some MSCs were cultured with L-ascorbic acid-2-phosphate (AsAP) and beta-glycerophosphate (beta-GP) or FK506 plus AsAP and beta-GP. The alkaline phosphatase (APase) activity and calcium deposition were detected 4, 8, 12, and 16 days after the culture. Scanning electron microscopy was used to examine the calcified nodules. Northern blotting was used to detect the mRNA expression of osteocalcium. Multiparous beta-tricalcium phosphate (beta-TCP) ceramic cubes were dipped into 2 kinds of suspension of MSCs, treated by FK506 + AsAP + beta-GP or AsAP + beta-GP, so as to produce 48 pieces of MSCs/beta-TCP complex that were randomly divided into 2 equal groups to be cultured with AsAP + beta-GP or AsAP + beta-GP + FK506 for 4 weeks. The these pieces were transplanted into the subcutaneous sites of the rats' backs and were taken out 4 and 8 weeks later respectively for histological examination. RESULTS: In vitro assays showed that the APase activity, calcium deposition, expression of osteocalcin mRNA of the FK506 + AsAP + beta-GP group at any time points were all significantly higher than those of the AsAP + beta-GP group (all P < 0.05). SEM showed that since the 16th day after culture calcified nodules began to be seen in the FK506 + AsAP + beta-GP group. Since the 4th weeks after transplantation remarkable new bone formation could be seen in the FK506 treated MSCs/beta-TCP complexes in comparison with those MSCs/beta-TCP complexes without treatment with FK506. CONCLUSION: Greatly enhancing the in vitro osteoblastic differentiation and in vivo osteogenesis of MSCs, FK506 has a potential value as a bone growth factor and may improve the clinical result of bone transplantation used to treat large bone defect. The results of this experiment also contributes to a better understanding on the mechanism of immunosuppressants.