Objective To investigate the relationship between sensitivity to cisplatin (DDP) and the expression of HSP70 in cervical cancer cells in vitro. Methods Cervical cancer Hela229 cells treated with different concentrations of DDP and the HSP70 inhibitor (PFT-μ) were examined for cell viability using MTT assay and colony forming ability. The cell apoptosis was analyzed by flow cytometry with propidium iodide staining and DAPI staining, and JC-1 staining was used to determine mitochondrial membrane potential. The expressions of HSP70, Bcl-2, Bax and caspase-3 were measured with Western blotting. A nude mouse model bearing Hela229 cell xenograft was used to evaluate the effect of DDP and PFT-μ on tumor growth. Results Hela229 cells expressed a higher level of HSP70 than normal cervical cells. The combined use of PFT-μ significantly enhanced the inhibitory effect of DDP (P<0.01) and increased the cell apoptosis in Hela229 cells. JC-1 staining demonstrated that DDP combined with PFT-μmore obviously reduced mitochondrial membrane potential. DDP combined with PFT-μmore strongly lowered Bcl-2 expression and increased the expressions of casepase-3 and Bax than DDP alone. In the nude mouse model, PFT-μ significantly enhanced DDP sensitivity of Hela229 cell xenografts (P<0.01). Conclusions Inhibition of HSP70 expression can enhance the sensitivity of cervical cancer cell to DDP both in vivo and in vitro possibly by promoting cell apoptosis, suggesting the potential of HSP70 as a new target for gene therapy of cervical cancer.

Objective To investigate the relationship between sensitivity to cisplatin (DDP) and the expression of HSP70 in cervical cancer cells in vitro. Methods Cervical cancer Hela229 cells treated with different concentrations of DDP and the HSP70 inhibitor (PFT-μ) were examined for cell viability using MTT assay and colony forming ability. The cell apoptosis was analyzed by flow cytometry with propidium iodide staining and DAPI staining, and JC-1 staining was used to determine mitochondrial membrane potential. The expressions of HSP70, Bcl-2, Bax and caspase-3 were measured with Western blotting. A nude mouse model bearing Hela229 cell xenograft was used to evaluate the effect of DDP and PFT-μ on tumor growth. Results Hela229 cells expressed a higher level of HSP70 than normal cervical cells. The combined use of PFT-μ significantly enhanced the inhibitory effect of DDP (P<0.01) and increased the cell apoptosis in Hela229 cells. JC-1 staining demonstrated that DDP combined with PFT-μmore obviously reduced mitochondrial membrane potential. DDP combined with PFT-μmore strongly lowered Bcl-2 expression and increased the expressions of casepase-3 and Bax than DDP alone. In the nude mouse model, PFT-μ significantly enhanced DDP sensitivity of Hela229 cell xenografts (P<0.01). Conclusions Inhibition of HSP70 expression can enhance the sensitivity of cervical cancer cell to DDP both in vivo and in vitro possibly by promoting cell apoptosis, suggesting the potential of HSP70 as a new target for gene therapy of cervical cancer.

Neurogenic bowel dysfunction (NBD) manifested as constipation and fecal incontinence often occurs after spinal cord injury (SCI).NBD affects patients' quality of life and is an urgent clinical problem to be solved.The mechanism of NBD is related to central and autonomic nervous system dysfunction,intestinal nervous system dysfunction,changes in intestinal microorganism composition and abnormal content of neurotransmitters.The evaluation method of NBD is mainly based on scoring and imaging,which lacks unified criteria,and the treatment method for NBD is the combination of traditional Chinese and Western medicine.The author summarizes the mechanism,evaluation method,treatment and nursing of NBD in order to provide new insight into these aspects to improve clinical efficacy.

After the articular cartilage injury, the metabolic level is increased during the progressive degeneration, the chondrocytes secrete a variety of inflammatory factors, and the original cell phenotype is gradually changed. For a long time, a large number of researchers have done a lot of researches to promote anabolism of chondrocytes and to maintain the stability of chondrocyte phenotype. There are many molecular signaling pathways involved in the process of promoting cartilage repair. This review focuses on the key signaling molecules in articular cartilage repair, such as transforming growth factor-beta and bone morphogenetic protein, and reveals their roles in the process of cartilage injury and repair, so that researchers in related fields can understand the molecular mechanism of cartilage injury and repair widely and deeply. Based on this, they may find promising targets and biological methods for the treatment of cartilage injury.
Bone Morphogenetic Proteins ; physiology ; Cartilage, Articular ; growth & development ; injuries ; Chondrocytes ; physiology ; Humans ; Regeneration ; Signal Transduction ; Transforming Growth Factor beta ; physiology