BACKGROUND: It is often difficult to determine the cause of low back pain (LBP) in the patients with lumbar disc herniation. The herniated disc has long been thought to be an important cause of the patient's complaint about LBP and sciatica. Whether the adjacent degenerative disc results in LBP needs further confirmations. OBJECTIVE: This study sought to determine whether the degenerative disc adjacent to the herniated disc in patients with LBP and radicular pain can result in discogenic LBP, as assessed by provocative discography, and to report the outcomes of the residual LBP when adjacent symptomatic disc were treated with methylene blue after microendoscopic discectomy. METHODS: Twenty lumbar disc herniation patients complaint about LBP and radicular pain underwent provocative discography. There was one degenerative herniated disc with one or more adjacent degenerative discs in their MRI. Provocative discography was performed on all degenerative discs and at least one normal disc for control. The severity of LBP and leg pain of all patients was assessed using visual analog scale before discography. All patients underwent microendoscopic discectomy at herniated level, and intradiscal injection of methylene blue was given at painful adjacent level in five patients after microendoscopic discectomy. RESULTS AND CONCLUSION: Discographies were performed on 64 discs of 20 patients, from L2-3 to L5-S1. There were 11 discs satisfying the positive response criteria, including 6 in degenerative segment adjacent to the herniated disc and 5 in the herniated disc that induced corresponding radiculopathy. The leg pains were evidently improved in all patients, while LBP was partially improved after microendoscopic discectomy. Six patients with symptomatic adjacent degenerative disc still had evident LBP, influencing their daily living. Five of them received intradiscal injection of methylene blue treatment and the LBP was relived. One patient refusing to the treatment still complained the LBP. Results evidenced that accompanying LBP for many LDH patients may come from the degenerative levels adjacent to the herniated disc.

Objective: To investigate the change in expression of anti-senescence marker protein calmodulin (RGN) in liver tissues of rats with immune hepatic fibrosis, and to observe the effect of compound glutathione inosine injection (CGII) on it. Methods: Rat liver fibrosis model was induced by intraperitoneal injection of porcine serum, and CGII intervention was administered at the appropriate time. Rat liver tissues were stained with HE and Masson. RGN and protein expression at mRNA in liver tissues was detected by fluorescence quantitative PCR and immunohistochemistry. One-way Anova was used for measurement data. LDS test was used for two-way comparison, and pathological semi-quantitative results were analyzed by rank-sum test. Results: The relative expression of RGN mRNA and protein in liver tissue of fibrotic rats was 82.23 ± 15.21 and 12.52 ± 3.23, respectively, which were significantly lower than that of normal rats 176.39 ± 11.35 and 59.23 ± 9.13 (P < 0.01). The degree of liver fibrosis in fibrotic rats after CGII intervention was significantly lower than fibrotic rats. The relative expression of RGN mRNA and protein in the intervention group was 168.78 ± 21.31 and 46.42 ± 4.71, respectively, which were significantly higher than fibrosis and spontaneous recovery group. The difference was statistically significant (P < 0.01). The relative expression of RGN mRNA and protein in the spontaneous recovery group was 86.23 ± 17.16 and 14.34 ± 5.16, which was higher than model group. The difference was not statistically significant (P > 0.05). Conclusion The expression of RGN in liver tissue of rats with hepatic fibrosis induced by porcine serum is decreased, while the expression of RGN increases with the decrease of fibrosis after CGII intervention, suggesting that the protein may play an important role in the development of liver fibrosis.

Objective: To investigate the effect and mechanism of XTP4 gene in apoptotic hepatoblastoma HepG2 cell line. Methods: HepG2 cells were transiently transfected with small interfering RNA of XTP4 genes, plasmid pcDNA3.1/myc-His(-) A-XTP4, and hepatitis B virus X protein transactivated x gene 4 (HBX protein trans-activate gene4, XTP4) and their respective negative controls. After 48h, the overexpression and interference expression condition of XTP4 in HepG2 cells were detected by Western blot. HepG2 cells apoptosis was detected by flow cytometry. The expression levels of apoptosis-related proteins P53, Bcl-2, Bax and Caspase-3 in HepG2 cells were detected by Western blot, and Bcl-2/Bax ratio was calculated. The chemiluminescence assay was used to detect activity of caspase-3 in HepG2 cells. The measured data were presented as ( ± s), and independent sample t-test was used for comparison between the two groups. Results: HepG2 cells had successfully achieved the overexpression and interference expression of XTP4 protein. Compared with the control group, the overexpression of XTP4 in HepG2 cells had significantly decreased the number of apoptotic cells (P < 0.05), and increased Bcl-2/Bax (P < 0.05) ratio, but decreased the expression of P53 protein (P < 0.05). The protein expression of Caspase-3 and activity of caspase-3 was decreased (P < 0.05). However, interference with XTP4 expression in HepG2 cells had significantly increased the number of apoptotic cells (P < 0.05) and decreased Bcl-2/Bax (P < 0.05) ratio, but increased the expression of P53 protein (P < 0.05). The protein expression of Caspase-3 and activity of caspase-3 was increased (P<0.05). Conclusion In HepG2 apoptosis XTP4 has inhibitory effect, and its effect on inhibiting HepG2 apoptosis may be achieved by regulating the Bcl-2/Bax ratio, and the P53 protein may be involved.