Nitidine chloride regulates cell function of bladder cancer in vitro through downregulating Lymphocyte antigen 75.

Nitidine chloride (NC) is effective on cancer in many tumors, but its effect on bladder cancer (BC) is unknown. We conducted cell function experiments to verify the antineoplastic effect of NC on BC cell lines (5637, T24, and UM-UC-3) in vitro. Then, mRNAs of NC-treated and NC-untreated BC cells were extracted for mRNA sequencing. Differentially expressed genes (DEGs), expression analysis, and drug molecular docking were conducted to discover the target gene of NC. Finally, functional enrichment was analyzed to explore the underlying mechanisms. NC dramatically inhibited proliferation, migration, and invasion, and it induced apoptosis and arrested the S and G2/M phases of BC cell lines. Lymphocyte antigen 75 (LY75) appeared to be the target of NC. LY75 was highly expressed and had the ability to distinguish BC tissue from non-cancerous tissue. Then, drug molecular docking confirmed the targeting relationship between NC and LY75. Gene enrichment analysis showed that the downregulated genes, after being treated with NC, were mainly enriched in pathways relevant to cell pathophysiological processes. NC inhibits BC cell proliferation, migration, and invasion, induces apoptosis, and arrests cell cycles by downregulating the expression of LY75. This study provides molecular and theoretical bases for NC treatment of BC.

[LUTS in BPH patients with histological prostatitis before and after transurethral resection of the prostate].

OBJECTIVE: To investigate the effects of transurethral resection of the prostate (TURP) on lower urinary tract symptoms (LUTS) in patients with benign prostatic hyperplasia (BPH) complicated by histological prostatitis. METHODS: This study included 432 cases of BPH pathologically confirmed after TURP. Excluding those with LUTS-related factors before and after surgery and based on the international prostatitis histological classification of diagnostic criteria, the remaining 144 cases were divided into groups A (pure BPH, n = 30), B (mild inflammation, n = 55), C (moderate inflammation, n = 31), and D (severe inflammation, n = 28). Each group was evaluated for LUTS by IPSS before and a month after surgery. RESULTS: A total of 399 cases (92.4%) were diagnosed as BPH with histological prostatitis, 269 (67.4%) mild, 86 (21.6%) moderate and 44 (11.0%) severe. The preoperative IPSS was 21.43 +/- 6.09 in group A, 21.75 +/- 5.97 in B, 27.84 +/- 4.18 in C and 31.00 +/- 2.92 in D, with statistically significant differences among different groups (P < 0.001) except between A and B (P = 1.000); the postoperative IPSS was 5.60 +/- 2.16 in A, 7.36 +/- 2.77 in B, 11.55 +/- 3.39 in C and 16.89 +/- 3.37 in D, with statistically significant differences among different groups (P < 0.01), and remarkably lower than the preoperative one (P < 0.001). Almost all the infiltrating inflammatory cells in BPH with histological prostatitis were lymphocytes. CONCLUSION: BPH is mostly complicated with histological chronic prostatitis. The severity of LUTS is higher in BPH patients with histological prostatitis than in those without before and after TURP, and positively correlated with the grade of inflammation. Those complicated with moderate or severe histological prostatitis should take medication for the management of LUTS.