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High-Fat Diet Induced Gut Microbiota Alterations Associating With Ghrelin/Jak2/Stat3 Up-Regulation to Promote Benign Prostatic Hyperplasia Development. Gu Meng,Liu Chong,Yang TianYe,Zhan Ming,Cai Zhikang,Chen Yanbo,Chen Qi,Wang Zhong Frontiers in cell and developmental biology The role of high-fat diet (HFD) induced gut microbiota alteration and Ghrelin as well as their correlation in benign prostatic hyperplasia (BPH) were explored in our study. The gut microbiota was analyzed by 16s rRNA sequencing. Ghrelin levels in serum, along with Ghrelin and Ghrelin receptor in prostate tissue of mice and patients with BPH were measured. The effect of Ghrelin on cell proliferation, apoptosis, and induction of BPH in mice was explored. Our results indicated that BPH mice have the highest ratio of Firmicutes and Bacteroidetes induced by HFD, as well as Ghrelin level in serum and prostate tissue was significantly increased compared with control. Elevated Ghrelin content in the serum and prostate tissue of BPH patients was also observed. Ghrelin promotes cell proliferation while inhibiting cell apoptosis of prostate cells. The effect of Ghrelin on enlargement of the prostate was found almost equivalent to that of testosterone propionate (TP) which may be attenuated by Ghrelin receptor antagonist YIL-781. Ghrelin could up-regulate Jak2/pJak2/Stat3/pStat3 expression and . Our results suggested that Gut microbiota may associate with Ghrelin which plays an important role in activation of Jak2/Stat3 in BPH development. Gut microbiota and Ghrelin might be pathogenic factors for BPH and could be used as a target for mediation. 10.3389/fcell.2021.615928
Epigallocatechin Gallate Attenuates Bladder Dysfunction via Suppression of Oxidative Stress in a Rat Model of Partial Bladder Outlet Obstruction. Gu Meng,Liu Chong,Wan Xiang,Yang Tianye,Chen Yanbo,Zhou Juan,Chen Qi,Wang Zhong Oxidative medicine and cellular longevity PURPOSE:To investigate the protective effect of epigallocatechin gallate (EGCG), a green tea extract, and its underlying mechanism on bladder dysfunction in a rat model of bladder outlet obstruction (BOO). MATERIALS AND METHODS:Sprague-Dawley rats of BOO were surgically induced and followed by treatment with EGCG (5 mg/kg/day) or saline (control) via intraperitoneal injection. Cystometry was performed on four weeks postoperatively in conscious rats. H&E, Masson trichrome, and TUNEL staining were performed to observe tissue alterations. Oxidative stress markers were measured, and protein expression of Nrf2-ARE pathway was examined by immunohistochemistry and Western blotting. RESULTS:Our data showed that EGCG could increase the peak voiding pressure and bladder compliance and prolong micturition interval of BOO rats compared with control and finally reduce the frequency of urinary. EGCG could ameliorate the increase of collagen fibers and ROS induced by obstruction and increase the activity of SOD, GSH-Px, and CAT. The level of cell apoptosis was decreased in BOO rats treated with EGCG compared with control, and caspase-3 expression was reduced as well. Moreover, EGCG could activate the Nrf2 expression with elevation of its target antioxidant proteins. CONCLUSIONS:EGCG alleviates BOO-induced bladder dysfunction via suppression of oxidative stress and activation of the protein expression of Nrf2-ARE pathway. 10.1155/2018/1393641
Serum indoxyl sulfate is associated with mortality in hospital-acquired acute kidney injury: a prospective cohort study. Wang Wenji,Hao Guihua,Pan Yu,Ma Shuai,Yang Tianye,Shi Peng,Zhu Qiuyu,Xie Yingxin,Ma Shaojun,Zhang Qi,Ruan Hong,Ding Feng BMC nephrology BACKGROUND:Protein-bound uremic toxins are associated with poor outcomes in patients with chronic kidney disease. The aim of this study is to investigate the relationship between indoxyl sulfate (IS), a protein-bound solute, and 90-day mortality in patients with acute kidney injury. METHODS:Adults with hospital-acquired AKI (HA-AKI) were enrolled in this prospective cohort study between 2014 and 2015, according to the KDIGO creatinine criteria. The primary end point was all-cause death during follow-up. RESULTS:The mean serum IS level in patients with HA-AKI was 2.74 ± 0.75 μg/ml, which was higher than that in healthy subjects (1.73 ± 0.11 μg/ml, P < 0.001) and critically ill patients (2.46 ± 0.35 μg/ml, P = 0.016) but was lower than that in patients with chronic kidney disease (3.07 ± 0.31 μg/ml, P < 0.001). Furthermore, serum IS levels (2.83 ± 0.55 μg/ml) remained elevated in patients with HA-AKI on the seventh day after AKI diagnosis. Patients with HA-AKI were divided into the following two groups according to the median serum IS level: the low-IS group and the high-IS group. A total of 94 (35.9%) patient deaths occurred within 90 days, including 76 (29.0%) in the low-IS group and 112 (42.7%) in the high-IS group (P = 0.019). Kaplan-Meier analysis revealed that the two groups differed significantly with respect to 90-day survival (log-rank P = 0.007), and Cox regression analysis showed that an IS level ≥ 2.74 μg/ml was significantly associated with a 2.0-fold increased risk of death (adjusted hazard ratio [HR], 2.92; 95% confidence interval [CI], 1.76 to 4.86; P < 0.001) compared with an IS level < 2.74 μg/ml. CONCLUSIONS:Serum IS levels were significantly elevated in patients with HA-AKI compared to those in healthy subjects and critically ill patients and were associated with a worse prognosis of HA-AKI. TRIAL REGISTRATION:www.clinicaltrials.gov NCT 00953992. Registered 6 August 2009. 10.1186/s12882-019-1238-9
Association between mineral and bone disorder in patients with acute kidney injury following cardiac surgery and adverse outcomes. Yang Tianye,Wang Wenji,Tang Xiao,Shi Peng,Zhang Lulu,Yu Wenyan,Xie Yingxin,Guo Daqiao,Ding Feng BMC nephrology BACKGROUND:Numerous studies have evaluated the prevalence and importance of mineral and bone disorders among patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD). However, little is known about dysregulated mineral and bone metabolism in acute kidney injury (AKI). METHODS:We evaluated the association between mineral and bone metabolites and clinical outcomes in 158 patients who underwent cardiac surgery and developed AKI between June 2014 and January 2016. The baseline characteristics of the patients were recorded, and the levels of mineral and bone metabolites, including calcium, phosphate, intact parathyroid hormone (iPTH), 25-hydroxyvitamin D (25D), bone-specific alkaline phosphatase (BAP), tartrate-resistant acid phosphatase 5b (TRACP-5b) and C-terminal fibroblast growth factor 23 (cFGF23) were measured within 12 h after establishing the clinical diagnosis. RESULTS:The serum phosphate, iPTH and cFGF23 levels were significantly associated with the 28-day mortality (phosphate: Hazard Ratio [HR] =2.620, 95% CI: 1.083 to 6.338, p = 0.035; iPTH: HR = 1.044, 95% CI: 1.001 to 1.090, p = 0.046; cFGF23: HR = 1.367, 95% CI: 1.168 to 1.599, p < 0.001). Moreover, higher serum cFGF23 and BAP levels were independently associated with an increased risk of adverse outcomes. Additionally, we found that the serum cFGF23 levels rose most significantly and were associated with the severity of AKI (P < 0.001). CONCLUSIONS:Mineral and bone metabolites are dysregulated and are associated with adverse clinical outcomes among patients with AKI. TRIAL REGISTRATION:www.clinicaltrials.gov NCT00953992. Registered 6 August 2009. 10.1186/s12882-019-1572-y