Fosfomycin tromethamine inhibits the expressions of TNF-α, IL-8 and IL-6 in the prostate tissue of rats with chronic bacterial prostatitis.

Wen-wei Cai; Dun-sheng MO; Ming Fan; Hong-cai Cai; Guo-wei Zhang; Wei-piong Wang; Xue-jun Shang

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Fosfomycin tromethamine inhibits the expressions of TNF-α, IL-8 and IL-6 in the prostate tissue of rats with chronic bacterial prostatitis.

Author: Wen-Wei CAI ¹ ; Dun-Sheng MO ² ; Ming FAN ³ ; Hong-Cai CAI ⁴ ; Guo-Wei ZHANG ⁵ ; Wei-Piong WANG ⁶ ; Xue-Jun SHANG ⁵
Author Information

1. Center of Reproductive Medicine, Jiaxing Women and Children's Hospital, Jiaxing, Zhejiang 314000, China.
2. Department of Urology, Liuzhou Workers' Hospital / The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi 545005, China.
3. .
4. Family Planning Research Institute / Center of Reproductive Medicine, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
5. Department of Andrology, Jinling Hospital Affiliated to Southern Medical University / Nanjing General Hospital of Nanjing Military Region, Nanjing, Jiangsu 210002, China.
6. Institute of Medical Laboratory, Jinling Hospital Affiliated to Southern Medical University / Nanjing General Hospital of Nanjing Military Region, Nanjing, Jiangsu 210002, China.
Publication Type:Journal Article
Keywords: chronic bacterial prostatitis; interleukin-6; interleukin-8; rat; tumor necrosis factor-α; fosfomycin tromethamine
MeSH: Animals; Anti-Bacterial Agents; pharmacology; Bacterial Infections; drug therapy; microbiology; Fosfomycin; pharmacology; Interleukin-6; metabolism; Interleukin-8; metabolism; Levofloxacin; pharmacology; Male; Prostate; drug effects; metabolism; Prostatitis; drug therapy; metabolism; Random Allocation; Rats; Rats, Sprague-Dawley; Tumor Necrosis Factor-alpha; metabolism
From:National Journal of Andrology 2018;24(6):491-498
CountryChina
Language:Chinese
Abstract:
ObjectiveTo investigate the effects of fosfomycin tromethamine (FT) on the expressions of tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), and interleukin-6 (IL-6) in the prostate tissue of the rats with chronic bacterial prostatitis (CBP).
METHODSWe randomly divided 70 male SD rats into 7 groups of equal number: blank control, CBP model control, positive control, 14 d low-dose FT, 7 d low-dose FT, 14 d high-dose FT, and 7 d high-dose FT. The CBP model rats in the latter five groups were treated intragastrically with levofloxacin at 100 mg/kg/d for 30 days and FT at 200 mg/kg/d for 14 and 7 days and at 300 mg/kg/d for 14 and 7 days, respectively. Then we collected the prostate tissue from the animals for determination of the levels of TNF-α, IL-8 and IL-6 by ELISA.
RESULTSCompared with the blank controls, the CBP model rats showed significantly increased levels of TNF-α (［19.83 ± 6.1］ vs ［32.93 ± 6.21］ ng/g prot, P <0.01), IL-8 (［8.26 ± 0.52］ vs ［16.2 ± 2.84］ ng/g prot, P <0.01) and IL-6 (［1.55 ± 0.11］ vs ［2.51 ± 1.06］ ng/g prot, P <0.05) in the prostate tissue. In comparison with the CBP model controls, the levels of TNF-α and IL-8 were remarkably decreased in the groups of positive control (［20.54 ± 5.78］ ng/g prot, P <0.01; ［12.43 ± 4.02］ ng/g prot, P <0.05), 14 d low-dose FT (［21.95 ± 6.48］ ng/g prot, P <0.01; ［11.11 ± 2.86］ ng/g prot, P <0.01), 7 d low-dose FT (［23.8 ± 6.93］ ng/g prot, P <0.05; ［12.43 ± 4.02］ ng/g prot, P <0.05), 14 d high-dose FT (［19.97 ± 2.58］ ng/g prot, P <0.01; ［8.83 ± 1.32］ ng/g prot, P <0.01), and 7 d high-dose FT (［21.97 ± 3.38］ ng/g prot, P <0.01; ［12.68±1.97］ ng/g prot, P <0.05). No statistically significant differences were observed between the positive control and FT groups in the contents of TNF-α, IL-8 or IL-6 (P >0.05). The expression of IL-6 was markedly reduced in the 14 d high-dose FT group as compared with the model controls (［1.76 ± 0.46］ vs ［2.51 ± 1.06］ ng/g prot, P<0.05) but exhibited no significant difference between the CBP model control and the other groups (P >0.05).
CONCLUSIONSFosfomycin tromethamine inhibits the expressions of TNF-α, IL-8 and IL-6 in the prostate tissue, suppresses its inflammatory reaction, promotes the repair of damaged prostatic structure, and thus contributes to the treatment of chronic bacterial prostatitis in rats.