Qianliexin capsule exerts anti‐inflammatory activity in chronic non‐bacterial prostatitis and benign prostatic hyperplasia via NF‐κB and inflammasome

Zang, Linghe; Tian, Fang; Yuan-cheng, Yao; Chen, Yiran; Shen, Yuxia; Han, Mingyu; Meng, Zhaoqing; Fan, Sheng-Ci; Zhang, Xinyi; Cai, Tian Quan; Gao, Qi; Zhang, Yuwei; Lu, Jincai

doi:10.1111/jcmm.16599

Cited by 27 publications

(25 citation statements)

References 45 publications

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“…The autophagy in prostate epithelial cells could be induced by the reduced secretion of IGF-1 from prostatic stromal cells after the treatment with finasteride [35]. Several herbal extracts, including Stauntonia hexaphylla and Qianliexin capsule, a standardized traditional Chinese herbal preparation, have been reported to induce autophagy and apoptosis in BPH in vivo [11,36]. In this study, we found that RWF extract could induce autophagic genes, ULK2 and SQSTM1/p62 at the transcriptional level in both BPH-1 and WPMY-1 cells.…”

Section: Discussionmentioning

confidence: 99%

Rauwolfia vomitoria extract suppresses benign prostatic hyperplasia by inducing autophagic apoptosis through endoplasmic reticulum stress

Huang

Xue

et al. 2022

BMC Complement Med Ther

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Background The current drug treatments for benign prostatic hyperplasia (BPH) have negative side effects. Therefore, it is important to find effective alternative therapies with significantly fewer side effects. Our previous study revealed that Rauwolfia vomitoria (RWF) root bark extract reversed BPH development in a rat model. However, the molecular mechanism of its inhibitory effects on BPH remains largely unknown. Methods BPH-1 and WPMY-1 cell lines derived from BPH epithelial and prostatic stromal compartments were selected to investigate how RWF extract inhibits BPH in vitro by MTT and flow cytometry assays. Microarray, quantitative real-time PCR, immunoblotting, and GFP-LC3 immunofluorescence assays were performed to evaluate the effects of RWF extract on endoplasmic reticulum stress (ER stress) and autophagic apoptosis pathways in two cell lines. A human BPH ex vivo explant assay was also employed for validation. Results RWF extract treatment decreased cell viability and induced apoptotic cell death in both BPH-1 and WPMY-1 cells in a concentration-dependent manner with the increase of pro-apoptotic PCDC4 protein. RWF extract induced autophagy by enhancing the levels of autophagic genes (ULK2 and SQSTM1/p62) and the LC3II:LC3I ratio, with the increase of GFP-LC3 puncta. Moreover, RWF extract activated PERK- and ATF6-associated ER stress pathways by inducing the transcriptional levels of EIF2AK3/PERK, DDIT3/CHOP and ATF6, accompanied by the reduction of BiP protein level, but not its mRNA level. Another ER stress pathway was not induced by RWF extract, as manifested by the lack of XBP1 splicing. Pharmacological inhibition of autophagy by 3-methyladenine abrogated apoptosis but not ER stress; while inhibition of ER stress by 4-phenylbutyrate alleviated the induction of autophagy and apoptosis. In addition, pretreatments with either 3-methyladenine or 4-phenylbutyrate suppressed RWF extract-induced cytotoxicity. Notably, the inductions of PERK- and ATF6-related stress pathways and autophagic apoptosis were confirmed in a human BPH ex vivo explant. Conclusions Our data have demonstrated that RWF extract significantly suppressed the viabilities of BPH epithelial cells and BPH myofibroblasts by inducing apoptosis via upregulating ER stress and autophagy. These data indicate that RWF extract is a potential novel alternative therapeutic approach for BPH.

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Section: Discussionmentioning

confidence: 99%

Rauwolfia vomitoria extract suppresses benign prostatic hyperplasia by inducing autophagic apoptosis through endoplasmic reticulum stress

Huang

Xue

et al. 2022

BMC Complement Med Ther

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“…The NF-κB signaling pathway, which seemed to be the imperative convergence of proinflammatory factors, has gradually become a research hotspot of BPA-triggered toxicity [ 48 , 49 ]. In the human prostatic epithelium, the inflammasome component NLRP3 activation controlled by NF-κB and ROS modulation could provoke the release of a series of proinflammatory factors and initiate an inflammatory cascade [ 50 ]. The BPA- and BPAF-driven ascended expression of and COX-2 in rat VP, as well as in human prostate cells, demonstrated that both of them hold promise as the potential interlocutors in mediating the prostatic hyperplasia disrupted by BPA and BPAF.…”

Section: Discussionmentioning

confidence: 99%

Individual and Combined Effect of Bisphenol A and Bisphenol AF on Prostate Cell Proliferation through NF-κB Signaling Pathway

Wang

Huang

Zhou

et al. 2022

IJMS

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The ubiquitous environmental endocrine disruptor bisphenol A (BPA) can induce prostatic dysfunction. However, to date, studies have focused little on the perturbations of prostate health initiated by the BPA derivative bisphenol AF (BPAF) and co-exposure to bisphenol compounds. An in vivo study orally administrated male rats with BPA (10, 90 μg/kg), BPAF (10, 90 μg/kg) and the inhibitor of nuclear transcription factor-κB (NF-κB), pyrrolidinedithiocarbamate (PDTC, 100 mg/kg). Based on the anatomical analysis, pathological observations and PCNA over-expression, we considered that low-dose BPA and BPAF facilitated ventral prostatic hyperplasia in rats. The results of IHC and ELISA mirrored the regulation of NF-κB p65, COX-2, TNF-α and EGFR in BPA- and BPAF-induced prostatic toxicity. An in vitro study found that the additive effect of combined exposure to BPA (10 nM) and BPAF (10 nM) could cause an elevation in the proliferation of and a reduction in the apoptosis level of human prostate stromal cells (WPMY−1) and fibroblasts (HPrF). Meanwhile, the underlying biomarkers of the NF-κB signaling pathway also involved the abnormal proliferative progression of prostate cells. The findings recapitulated the induction of BPAF exposure and co-treatment with BPA and BPAF on prostatic hyperplasia and emphasized the modulation of the NF-κB signaling pathway.

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“…While in the experimental autoimmune prostatitis (EAP) mouse model, apart from the attenuating effect of the NLRP3 inhibitor MCC950 ( 67 ), melatonin also inhibited the NLRP3 inflammasome signaling pathway by activating Sirt1, which reduced prostate inflammation and pelvic pain ( 68 ). Zang et al found elevated expression of NLRP3, Caspase-1 and ASC in CNP rats, and Qianliexin capsule (QLX) suppressed the high expression of these proteins ( 69 ). Another study showed that the levels of Caspase-1 and Pyrin domain containing proteins 1 and 3 (NALP1 and NALP3) were increased in local carrageenan-induced prostate inflammation ( 70 ).…”

Section: Pyroptosis In Prostate Diseasementioning

confidence: 99%

Relationship between pyroptosis-mediated inflammation and the pathogenesis of prostate disease

Zhao

Guo²,

Gao³

et al. 2023

Front. Med.

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The largest solid organ of the male genitalia, the prostate gland, is comprised of a variety of cells such as prostate epithelial cells, smooth muscle cells, fibroblasts, and endothelial cells. Prostate diseases, especially prostate cancer and prostatitis, are often accompanied by acute/chronic inflammatory responses or even cell death. Pyroptosis, a cell death distinct from necrosis and apoptosis, which mediate inflammation may be closely associated with the development of prostate disease. Pyroptosis is characterized by inflammasome activation via pattern recognition receptors (PRR) upon recognition of external stimuli, which is manifested downstream by translocation of gasdermin (GSDM) protein to the membrane to form pores and release of inflammatory factors interleukin (IL)-1β and IL-18, a process that is Caspase-dependent. Over the past number of years, many studies have investigated the role of inflammation in prostate disease and have suggested that pyroptosis may be an important driver. Understanding the precise mechanism is of major consequence for the development of targeted therapeutic strategies. This review summarizes the molecular mechanisms, regulation, and cellular effects of pyroptosis briefly and then discuss the current pyroptosis studies in prostate disease research and the inspiration for us.

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Qianliexin capsule exerts anti‐inflammatory activity in chronic non‐bacterial prostatitis and benign prostatic hyperplasia via NF‐κB and inflammasome

Cited by 27 publications

References 45 publications

Rauwolfia vomitoria extract suppresses benign prostatic hyperplasia by inducing autophagic apoptosis through endoplasmic reticulum stress

Rauwolfia vomitoria extract suppresses benign prostatic hyperplasia by inducing autophagic apoptosis through endoplasmic reticulum stress

Individual and Combined Effect of Bisphenol A and Bisphenol AF on Prostate Cell Proliferation through NF-κB Signaling Pathway

Relationship between pyroptosis-mediated inflammation and the pathogenesis of prostate disease

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