Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a complex disease that is often accompanied by mental health disorders. However, the potential mechanisms underlying the heterogeneous clinical presentation of CP/CPPS remain uncertain. This study analyzed widely targeted metabolomic data of expressed prostatic secretions (EPS) and plasma to reveal the underlying pathological mechanisms of CP/CPPS. A total of 24 CP/CPPS patients from The Second Nanning People's Hospital (Nanning, China), and 35 asymptomatic control individuals from First Affiliated Hospital of Guangxi Medical University (Nanning, China) were enrolled. The indicators related to CP/CPPS and psychiatric symptoms were recorded. Differential analysis, coexpression network analysis, and correlation analysis were performed to identify metabolites that were specifically altered in patients and associated with various phenotypes of CP/CPPS. The crucial links between EPS and plasma were further investigated. The metabolomic data of EPS from CP/CPPS patients were significantly different from those from control individuals. Pathway analysis revealed dysregulation of amino acid metabolism, lipid metabolism, and the citrate cycle in EPS. The tryptophan metabolic pathway was found to be the most significantly altered pathway associated with distinct CP/CPPS phenotypes. Moreover, the dysregulation of tryptophan and tyrosine metabolism and elevation of oxidative stress-related metabolites in plasma were found to effectively elucidate the development of depression in CP/CPPS. Overall, metabolomic alterations in the EPS and plasma of patients were primarily associated with oxidative damage, energy metabolism abnormalities, neurological impairment, and immune dysregulation. These alterations may be associated with chronic pain, voiding symptoms, reduced fertility, and depression in CP/CPPS. This study provides a local-global perspective for understanding the pathological mechanisms of CP/CPPS and offers potential diagnostic and therapeutic targets.
Humans ; Male ; Prostatitis/blood* ; Adult ; Pelvic Pain/blood* ; Metabolomics ; Prostate/metabolism* ; Middle Aged ; Chronic Pain/blood* ; Metabolome ; Case-Control Studies ; Tryptophan/blood* ; Depression/blood* ; Oxidative Stress/physiology* ; Chronic Disease ; Lipid Metabolism/physiology*

OBJECTIVE: To investigate the clinical efficacy of Huang'e Capsules in the treatment of type ⅢA chronic prostatitis, and its effects on the levels of the inflammatory cytokines neutrophil elastase (NE), IL-8 and TGF-β1 in the expressed prostatic secretion (EPS) of the patients. METHODS: We selected 120 patients with type ⅢA chronic prostatitis and randomly assigned them to medication with Huang'e Capsules (the trial group, n = 60) or Levofloxacin and Tamsulosin (the control group, n = 60), both for a course of 4 weeks. We obtained the NIH-CPSI scores and the levels of NE, IL-8 and TGF-β1 in the EPS, and compared them between the two groups before and after treatment. RESULTS: Totally, 116 of the patients completed the study, 59 in the trial and 57 in the control group. The overall clinical effectiveness was significantly higher in the trial group than in the control (89.8% vs 77.2%, P<0.05). Compared with the baseline, the patients of the trial group showed significant decreases after treatment in the total NIH-CPSI scores (32.5±7.4 vs 13.2±5.1), pain symptom scores (13.7±3.9 vs 4.2±2.3), urination symptom scores (6.9±2.4 vs 5.1±3.2) and quality of life (QOL) scores (8.3±2.7 vs 3.7±1.5) (all P< 0.05), and so did the controls in the total NIH-CPSI scores (30.8±7.8 vs 13.7±3.9), pain symptom scores (14.2±4.1 vs 7.8±2.9), urination symptom scores (7.1±2.7 vs 4.9±3.4) and quality of life (QOL) scores (8.1±2.4 vs 5.6±1.9) (all P< 0.05), and the decreases were even more significant in the trial than in the control group in the pain symptom and QOL scores ( P< 0.05). The patients of the trial group also exhibited a marked reduction after treatment in the contents of NE (［1135.4±321.5］ vs ［347.6±207.3］ ng/L, P< 0.05) and IL-8 (［974.9±231.6］ vs ［ 431.3±207.2］ ng/L, P< 0.05) but an elevation in that of TGF-β1 (［591.0±172.1］ vs ［1 402.1 ± 221.5］ ng/L, P< 0.05) in the EPS, and so did the controls in the levels of NE (［1052.8±280.3］ vs ［761.1±225.1］ ng/L, P<0.05), (［1007.5±287.7］ vs ［775.7±182.5］ ng/L, P< 0.05), (［607.8±201.3］ vs ［871.3±192.5］ ng/L, P< 0.05), with even more significant improvement in the trial than in the control group (P< 0.05). CONCLUSION Huang'e Capsules has a significant clinical efficacy and safety in the treatment of type IIIA prostatitis, which can effectively relieve the pain and urination symptoms and improve the levels of the inflammatory cytokines NE, IL-8 and TGF-β1 in the patients.
Humans ; Male ; Prostatitis/metabolism* ; Interleukin-8/metabolism* ; Drugs, Chinese Herbal/therapeutic use* ; Transforming Growth Factor beta1/metabolism* ; Prostate/metabolism* ; Leukocyte Elastase/metabolism* ; Tamsulosin ; Treatment Outcome ; Capsules ; Middle Aged ; Phytotherapy ; Cytokines/metabolism* ; Adult ; Levofloxacin

Experimental autoimmune prostatitis (EAP)-induced persistent inflammatory immune response can significantly upregulate the expression of N-methyl-D-aspartic acid (NMDA) receptors in the paraventricular nucleus (PVN). However, the mechanism has not yet been elucidated. Herein, we screened out the target prostate-derived inflammation cytokines (PDICs) by comparing the inflammatory cytokine levels in peripheral blood and cerebrospinal fluid (CSF) between EAP rats and their controls. After identifying the target PDIC, qualified males in initial copulatory behavior testing (CBT) were subjected to implanting tubes onto bilateral PVN. Next, they were randomly divided into four subgroups (EAP-1, EAP-2, Control-1, and Control-2). After 1-week recovery, EAP-1 rats were microinjected with the target PDIC inhibitor, Control-1 rats were microinjected with the target PDIC, while the EAP-2 and Control-2 subgroups were only treated with the same amount of artificial CSF (aCSF). Results showed that only interleukin-1β(IL-1β) had significantly increased mRNA-expression in the prostate of EAP rats compared to the controls (P < 0.001) and significantly higher protein concentrations in both the serum (P = 0.001) and CSF (P < 0.001) of the EAP groups compared to the Control groups. Therefore, IL-1β was identified as the target PDIC which crosses the blood-brain barrier, thereby influencing the central nervous system. Moreover, the EAP-1 subgroup displayed a gradually prolonged ejaculation latency (EL) in the last three CBTs (all P < 0.01) and a significantly lower expression of NMDA NR1 subunit in the PVN (P = 0.043) compared to the respective control groups after a 10-day central administration of IL-1β inhibitors. However, the Control-1 subgroup showed a gradually shortened EL (P < 0.01) and a significantly higher NR1 expression (P = 0.004) after homochronous IL-1β administration. Therefore, we identified IL-1β as the primary PDIC which shortens EL in EAP rats. However, further studies should be conducted to elucidate the specific molecular mechanisms through which IL-1β upregulates NMDA expression.
Animals ; Cytokines/metabolism* ; Disease Models, Animal ; Ejaculation/physiology* ; Interleukin-1beta/metabolism* ; Male ; N-Methylaspartate/metabolism* ; Prostate/metabolism* ; Prostatitis/metabolism* ; Rats ; Receptors, N-Methyl-D-Aspartate/metabolism*

We investigated the therapeutic effects of superoxide dismutase (SOD) from thermophilic bacterium HB27 on chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) and its underlying mechanisms. A Sprague-Dawley rat model of CP/CPPS was prepared and then administered saline or Thermus thermophilic (Tt)-SOD intragastrically for 4 weeks. Prostate inflammation and fibrosis were analyzed by hematoxylin and eosin staining, and Masson staining. Alanine transaminase (ALT), aspartate transaminase (AST), serum creatinine (CR), and blood urea nitrogen (BUN) levels were assayed for all animals. Enzyme-linked immunosorbent assays (ELISA) were performed to analyze serum cytokine concentrations and tissue levels of malondialdehyde, nitric oxide, SOD, catalase, and glutathione peroxidase. Reactive oxygen species levels were detected using dichlorofluorescein diacetate. The messenger ribonucleic acid (mRNA) expression of tissue cytokines was analyzed by reverse transcription polymerase chain reaction (RT-PCR), and infiltrating inflammatory cells were examined using immunohistochemistry. Nuclear factor-κB (NF-κB) P65, P38, and inhibitor of nuclear factor-κBα (I-κBα) protein levels were determined using western blot. Tt-SOD significantly improved histopathological changes in CP/CPPS, reduced inflammatory cell infiltration and fibrosis, increased pain threshold, and reduced the prostate index. Tt-SOD treatment showed no significant effect on ALT, AST, CR, or BUN levels. Furthermore, Tt-SOD reduced inflammatory cytokine expression in prostate tissue and increased antioxidant capacity. This anti-inflammatory activity correlated with decreases in the abundance of cluster of differentiation 3 (CD3), cluster of differentiation 45 (CD45), and macrophage inflammatory protein 1α (MIP1α) cells. Tt-SOD alleviated inflammation and oxidative stress by reducing NF-κB P65 and P38 protein levels and increasing I-κBα protein levels. These findings support Tt-SOD as a potential drug for CP/CPPS.
Animals ; Chronic Pain ; Cytokines/metabolism* ; Fibrosis ; Humans ; Inflammation/metabolism* ; Male ; NF-kappa B/metabolism* ; Pelvic Pain/pathology* ; Prostatitis/metabolism* ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; Syndrome

MicroRNAs (miRNAs) are considered to be involved in the pathogenic initiation and progression of chronic nonbacterial prostatitis (CNP); however, the comprehensive expression profile of dysregulated miRNAs, relevant signaling pathways, and core machineries in CNP have not been fully elucidated. In the current research, CNP rat models were established through the intraprostatic injection of carrageenan into the prostate. Then, next-generation sequencing was performed to explore the miRNA expression profile in CNP. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) bioinformatical analyses were conducted to reveal the enriched biological processes, molecular functions, and cellular components and signaling pathways. As a result, 1224, 1039, and 1029 known miRNAs were annotated in prostate tissues from the blank control (BC), normal saline injection (NS), and carrageenan injection (CAR) groups (n = 3 for each group), respectively. Among them, 84 miRNAs (CAR vs BC) and 70 miRNAs (CAR vs NS) with significantly different expression levels were identified. Compared with previously reported miRNAs with altered expression in various inflammatory diseases, the majority of deregulated miRNAs in CNP, such as miR-146b-5p, miR-155-5p, miR-150-5p, and miR-139-5p, showed similar expression patterns. Moreover, bioinformatics analyses have enriched mitogen-activated protein kinase (MAPK), cyclic adenosine monophosphate (cAMP), endocytosis, mammalian target of rapamycin (mTOR), and forkhead box O (FoxO) signaling pathways. These pathways were all involved in immune response, which indicates the critical regulatory role of the immune system in CNP initiation and progression. Our investigation has presented a global view of the differentially expressed miRNAs and potential regulatory networks containing their target genes, which may be helpful for identifying the novel mechanisms of miRNAs in immune regulation and effective target-specific theragnosis for CNP.
Animals ; Computational Biology ; Databases, Genetic ; Gene Expression Profiling ; High-Throughput Nucleotide Sequencing ; Male ; MicroRNAs/metabolism* ; Prostate/metabolism* ; Prostatitis/metabolism* ; Rats ; Rats, Wistar

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.

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

This study aims to validate our hypothesis that acid-sensing ion channels (ASICs) may contribute to the symptom of pain in patients with chronic prostatitis (CP). We first established a CP rat model, then isolated the L5-S2 spinal dorsal horn neurons for further studies. ASIC1a was knocked down and its effects on the expression of neurogenic inflammation-related factors in the dorsal horn neurons of rat spinal cord were evaluated. The effect of ASIC1a on the Ca²⁺ ion concentration in the dorsal horn neurons of rat spinal cord was measured by the intracellular calcium ([Ca²⁺]i) intensity. The effect of ASIC1a on the p38/mitogen-activated protein kinase (MAPK) signaling pathway was also determined. ASIC1a was significantly upregulated in the CP rat model as compared with control rats. Acid-induced ASIC1a expression increased [Ca²⁺]i intensity in the dorsal horn neurons of rat spinal cord. ASIC1a also increased the levels of neurogenic inflammation-related factors and p-p38 expression in the acid-treated dorsal horn neurons. Notably, ASIC1a knockdown significantly decreased the expression of pro-inflammatory cytokines. Furthermore, the levels of p-p38 and pro-inflammatory cytokines in acid-treated dorsal horn neurons were significantly decreased in the presence of PcTx-1, BAPTA-AM, or SB203580. Our results showed that ASIC1a may contribute to the symptom of pain in patients with CP, at least partially, by regulating the p38/MAPK signaling pathway.
Acid Sensing Ion Channel Blockers/pharmacology* ; Acid Sensing Ion Channels/genetics* ; Animals ; Calcium/metabolism* ; Chelating Agents/pharmacology* ; Chronic Disease ; Cytokines/metabolism* ; Disease Models, Animal ; Egtazic Acid/pharmacology* ; Gene Knockdown Techniques ; Imidazoles/pharmacology* ; Inflammation/metabolism* ; MAP Kinase Signaling System/genetics* ; Male ; Pain/genetics* ; Peptides/pharmacology* ; Phosphorylation/drug effects* ; Posterior Horn Cells/metabolism* ; Prostatitis/complications* ; Protein Kinase Inhibitors/pharmacology* ; Pyridines/pharmacology* ; Rats ; Spider Venoms/pharmacology* ; Up-Regulation ; p38 Mitogen-Activated Protein Kinases/metabolism*

Objective: To investigate the role of mast cells in chronic prostatitis / chronic pelvic pain syndrome (CP/CPPS). METHODS: Forty-five male SD rats were equally randomized into a control, an experimental autoimmune prostatitis (EAP) model, and an intervention group. The EAP model was made in the latter two groups by subcutaneous injection of mixed suspension of complete Freund's adjuvant and prostate tissue, while the controls were treated subcutaneously with 0.9% sodium chloride. Tactile allodynia was quantified in the pelvic region of the control and EAP animals using Von-Frey filaments at 5, 10, 20, 30 and 40 days. After successful establishment of the EAP model, the rats of the intervention group were injected intraperitonieally with cromolyn sodium for 10 days, and meanwhile tactile allodynia was detected in the rats of the intervention and EAP model groups every other day. Then the prostates of the rats were harvested for HE and toluidine blue staining and measurement of the expression of mast cell tryptase by immunohistochemistry and Western blot. RESULTS: Von-Frey assessment showed a more severe pelvic pain in the EAP model than in the control rats, but milder in the intervention group than in the EAP models. HE staining revealed infiltration of lymphocytes and neutrophils in the prostate and congestion surrounding the gland in the EAP model rats, but none in the controls. However, both the infiltration and congestion were significantly alleviated in the intervention group. Toluidine blue staining shown that. Compared with the control group, the total count of mast cells and the number degranulated mast cells were markedly increased in the EAP models (P <0.01) but decreased in the intervention group (P <0.05). Both immunohistochemistry and Western blot manifested that the expression of tryptase in the mast cells was remarkably upregulated in the EAP (both P <0.01) but down-regulated in the intervention group (P <0.05 and P <0.01). CONCLUSIONS Both the total count of mast cells and the number of degranulated mast cells are significantly increased in the prostate of EAP rats. Mast cells are one of the most important mediators of type Ⅲ prostatitis-induced chronic pelvic pain, which can be used as a target for the intervention and treatment of type Ⅲ prostatitis.
Adjuvants, Immunologic ; Animals ; Autoimmune Diseases ; etiology ; pathology ; Cell Degranulation ; Chronic Disease ; Chronic Pain ; etiology ; Disease Models, Animal ; Freund's Adjuvant ; Male ; Mast Cells ; enzymology ; physiology ; Pelvic Pain ; etiology ; Prostatitis ; etiology ; pathology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Tryptases ; metabolism

Objective: To investigate the effect of waist hot-compress with the Shirexiao (SRX) pad on the expressions of Th17/Treg-specific factors in the prostatic tissue of the mouse model of experimental autoimmune prostatitis (EAP) with damp heat syndrome, and explore its possible action mechanisms. METHODS: Twenty healthy male mice were included as normal controls and another 100 chosen for establishing the model of EAP with damp heat syndrome by subcutaneous injection of purified prostate protein solution from the Wistar rat and Freund's complete adjuvant using the TCM method. The model mice were randomly divided into five groups: model control, matrix, and low-, medium- and high-dose SRX. After chemical removal of the hair at lumbar vertebrae 1－3, the animals of the low-, medium- and high-dose SRX groups were treated with the SRX pad heated to 45℃ and externally applied to the non-hair area, qd, bid, and tid, respectively, 10 minutes each time, those of the matrix group with the vaseline pad, and those of the normal and model control groups with the saline pad. After 4 weeks of continuous treatment, all the mice were sacrificed for determination of the protein and mRNA expressions of RORγt and Foxp3 in the prostate tissue by Western blot and quantitative real-time PCR. RESULTS: The symptoms, signs and pathological changes of the EAP model mice were similar to the manifestations of chronic prostatitis. After intervention, the protein and mRNA expressions of Foxp3 were significantly down-regulated while those of RORγt markedly up-regulated in the EAP model group as compared with the normal control (P <0.05). In comparison with the model controls, the protein and mRNA expressions of RORγt were remarkably decreased in the medium- and high-dose SRX groups (P <0.05), that of the Foxp3 protein was markedly increased in the high-dose group (P <0.05), while that of Foxp3 mRNA exhibited no statistically significant difference in the low-, medium- or high-dose groups (P >0.05). CONCLUSIONS The Shirexiao waist hot-compress therapy plays a positive role in the treatment of autoimmune prostatitis with damp heat syndrome by reducing the expression of RORγt, inhibiting the differentiation of Th17 and thus checking the differentiation imbalance of Th17/Treg.
Adjuvants, Immunologic ; Animals ; Compression Bandages ; Disease Models, Animal ; Drugs, Chinese Herbal ; Forkhead Transcription Factors ; metabolism ; Freund's Adjuvant ; Hair Removal ; Hot Temperature ; Humans ; Male ; Mice ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; metabolism ; Prostatitis ; etiology ; metabolism ; RNA, Messenger ; metabolism ; Random Allocation ; Rats ; Rats, Wistar ; T-Lymphocytes, Regulatory ; metabolism ; Th17 Cells ; metabolism ; Up-Regulation

Objective: To observe the effects of swimming plus medication on the expressions of cytokines in rats with chronic abacterial prostatitis (CAP). METHODS: Forty healthy adult male SD rats were randomly divided into five groups of equal number, normal control, CAP model control, medication, exercise therapy, and exercise + medication. The CAP model was made by Xiaozhiling injection, and at 7 days after modeling, the rats in the medication and exercise + medication groups were treated intragastrically with Qianlie Shutong Capsules (0.016 g/ml) at 20 ml per kg of the body weight qd, those in the exercise therapy and exercise + medication groups were made swim at a regular time once a day, 35 minutes on the first day and 5 minutes more on the second until 50 minutes once, for 4 successive weeks, and those in the normal control, model control and exercise therapy groups received normal saline only. After 14 and 28 days of treatment, all the rats were killed and their prostates harvested for observation of histopathological changes and determination of the expressions of TNF- α, IL-1β and IL-6 in the prostatic tissue homogenate by ELISA. RESULTS: After 14 days of treatment, the expression levels of TNF-α, IL-1β and IL-6 were significantly elevated in the groups of CAP model control (［183.08±8.07］ pg/ml, ［57.55±3.53］ pg/ml and ［256.15±13.95］ ng/L), medication (［118.49±8.06］ pg/ml, ［42.64±4.64 ］ pg/ml and ［200.74±9.33］ ng/L), exercise therapy (［169.63±10.64］ pg/ml, ［50.45±5.71］ pg/ml and ［245.23±6.49］ ng/L), and exercise + medication (［107.82±7.81］ pg/ml, ［40.35±6.93］ pg/ml and ［187.04±10.85］ ng/L) as compared with those in the normal control (［20.36±1.82］ pg/ml, ［14.64±1.91］ pg/ml and ［70.58±2.09］ ng/L) (P<0.05). At 28 days, the levels of TNF- α, IL-1β, IL-6 were remarkably lower in the exercise + medication group (［29.30±3.78］ pg/ml, ［16.91±1.24］ pg/ml and ［ 88.65±6.74］ ng/L) than in the medication group (［39.67±3.19］ pg/ml, ［26.27±3.49］ pg/ml and ［110.26±6.33］ ng/L) (P<0.05) and close to those of the normal control group (［19.34±1.76］ pg/ml, ［13.68±1.06］ pg/ml and ［71.34±2.50］ ng/L). During the treatment, no obvious pathological changes were found in the prostate tissue of the normal control rats, while significant chronic prostatic inflammation was observed in the CAP models, and the inflammation was relieved in different degrees after intervention, most significantly in the exercise + medication group. CONCLUSIONS Swimming can relieve prostatic inflammation and swimming plus medication can effectively reduce the expressions of cytokines and alleviate histological damage in the prostatic tissue of CAP rats.
Animals ; Chronic Disease ; Combined Modality Therapy ; methods ; Cytokines ; metabolism ; Drugs, Chinese Herbal ; therapeutic use ; Interleukin-1beta ; metabolism ; Interleukin-6 ; metabolism ; Male ; Physical Conditioning, Animal ; Prostatitis ; metabolism ; therapy ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Swimming ; Time Factors ; Tumor Necrosis Factor-alpha ; metabolism