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  1. Article ; Online: Ba-Wei-Die-Huang-Wan (Hachimi-jio-gan) can ameliorate ketamine-induced cystitis by modulating neuroreceptors, inflammatory mediators, and fibrogenesis in a rat model.

    Lee, Wei-Chia / Tain, You-Lin / Chuang, Yao-Chi / Tsai, Cheng-Nan / Yu, Chun-Chieh / Su, Chia-Hao

    Neurourology and urodynamics

    2019  Volume 38, Issue 8, Page(s) 2159–2169

    Abstract: Aim: We investigated the effects of Ba-Wei-Die-Huang-Wan (BWDHW) on ketamine-induced cystitis (KIC) in a rat model.: Methods: Female Sprague-Dawley rats were distributed into three groups: control (saline), ketamine (25 mg/kg/day for 28 days), or ... ...

    Abstract Aim: We investigated the effects of Ba-Wei-Die-Huang-Wan (BWDHW) on ketamine-induced cystitis (KIC) in a rat model.
    Methods: Female Sprague-Dawley rats were distributed into three groups: control (saline), ketamine (25 mg/kg/day for 28 days), or ketamine (25 mg/kg/day for 28 days) plus BWDHW (90 mg/kg/day, started from day 14). Functional magnetic resonance imaging (fMRI), metabolic cage study, and cystometry were evaluated. Bladder histology was evaluated. Western blots of the bladder proteins were carried out.
    Results: Compared with controls, ketamine-treated rats showed stronger fMRI intensity in the periaqueductal gray area and bladder overactivity in the bladder functional study, but the ketamine/BWDHW-treated rats did not. Furthermore, ketamine breached the uroplakin III membrane at the apical surface of the urothelium, enhanced substance P spread over the urothelium, induced suburothelial hemorrhage and monocyte/macrophage infiltration, and caused interstitial fibrosis deposition. By contrast, the BWDHW-treated rats exhibited less substance P spread, lower suburothelial monocyte/macrophage infiltration, and lower interstitial fibrosis deposition. The ketamine group showed significant overexpression of neuroreceptors in the bladder mucosa (the transient receptor potential vanilloid 1 and M
    Conclusion: BWDHW could exert therapeutic effects by inhibiting the upregulation of neuroreceptors, modulating inflammatory mediators, suppressing fibrogenesis, and ameliorating bladder overactivity in rats with KIC.
    MeSH term(s) Animals ; Collagen/drug effects ; Collagen/metabolism ; Cyclooxygenase 2/drug effects ; Cyclooxygenase 2/metabolism ; Cystitis/chemically induced ; Cystitis/metabolism ; Cystitis/pathology ; Cystitis/physiopathology ; Drugs, Chinese Herbal/pharmacology ; Female ; Fibronectins/drug effects ; Fibronectins/metabolism ; Functional Neuroimaging ; Intercellular Adhesion Molecule-1/drug effects ; Intercellular Adhesion Molecule-1/metabolism ; Interleukin-1beta/drug effects ; Interleukin-1beta/metabolism ; Interleukin-6/metabolism ; Ketamine/adverse effects ; Magnetic Resonance Imaging ; NF-kappa B/drug effects ; NF-kappa B/metabolism ; Periaqueductal Gray/diagnostic imaging ; Rats ; Rats, Sprague-Dawley ; Receptors, Muscarinic/drug effects ; Receptors, Muscarinic/metabolism ; Sensory Receptor Cells ; Substance P/drug effects ; Substance P/metabolism ; TRPV Cation Channels/drug effects ; TRPV Cation Channels/metabolism ; Transforming Growth Factor beta1/drug effects ; Transforming Growth Factor beta1/metabolism ; Tumor Necrosis Factor-alpha/drug effects ; Tumor Necrosis Factor-alpha/metabolism ; Urinary Bladder/drug effects ; Urinary Bladder/metabolism ; Urinary Bladder/pathology ; Urinary Bladder/physiopathology ; Urinary Bladder, Overactive/chemically induced ; Urinary Bladder, Overactive/metabolism ; Urinary Bladder, Overactive/pathology ; Urinary Bladder, Overactive/physiopathology ; Urothelium/drug effects ; Urothelium/metabolism
    Chemical Substances Drugs, Chinese Herbal ; Fibronectins ; IL1B protein, rat ; Il6 protein, rat ; Interleukin-1beta ; Interleukin-6 ; NF-kappa B ; Receptors, Muscarinic ; TRPV Cation Channels ; TRPV1 receptor ; Tgfb1 protein, rat ; Transforming Growth Factor beta1 ; Tumor Necrosis Factor-alpha ; hachimijiogan ; Intercellular Adhesion Molecule-1 (126547-89-5) ; Substance P (33507-63-0) ; Ketamine (690G0D6V8H) ; Collagen (9007-34-5) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Ptgs2 protein, rat (EC 1.14.99.1)
    Language English
    Publishing date 2019-09-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 604904-7
    ISSN 1520-6777 ; 0733-2467
    ISSN (online) 1520-6777
    ISSN 0733-2467
    DOI 10.1002/nau.24165
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Potential Orphan Drug Therapy of Intravesical Liposomal Onabotulinumtoxin-A for Ketamine-Induced Cystitis by Mucosal Protection and Anti-inflammation in a Rat Model.

    Lee, Wei-Chia / Su, Chia-Hao / Tain, You-Lin / Tsai, Cheng-Nan / Yu, Chun-Chieh / Chuang, Yao-Chi

    Scientific reports

    2018  Volume 8, Issue 1, Page(s) 5795

    Abstract: Ketamine abusers may develop ulcerative cystitis and severe lower urinary tract symptoms, which is a medical dilemma. Recently, researchers have found the endemic of ketamine-induced cystitis worldwide. The intravesical administration of liposome- ... ...

    Abstract Ketamine abusers may develop ulcerative cystitis and severe lower urinary tract symptoms, which is a medical dilemma. Recently, researchers have found the endemic of ketamine-induced cystitis worldwide. The intravesical administration of liposome-encapsulated onabotulinumtoxinA (Lipotoxin) might facilitate the healing of the damaged urothelium from liposomes, and reduce the urinary symptoms by onabotulinumtoxinA-induced chemo-denervation. Using female Sprague-Dawley rats, we investigated the effects of Lipotoxin on ketamine-induced cystitis. Functional magnetic resonance imaging, metabolic cage study, and cystometry were conducted. Paraffin-embedded sections were stained. The bladder mucosa and muscle proteins were assessed through Western blotting. We observed that repeated intravesical Lipotoxin instillation could improve suburothelial hemorrhage, recover the urothelial tight junction and adhesion proteins (zonula occludens-1 and E-cadherin), ensure less substance P in the urothelium, inhibit the overexpression of inflammatory mediators (IL-6, TNF-α, nuclear NF-κB, and COX-2) in the detrusor, suppress the upregulation of the mucosal TRPV1 and detrusor M
    MeSH term(s) Administration, Intravesical ; Analgesics/adverse effects ; Animals ; Anti-Inflammatory Agents/administration & dosage ; Botulinum Toxins, Type A/administration & dosage ; Cystitis/chemically induced ; Cystitis/diagnostic imaging ; Cystitis/drug therapy ; Cystitis/pathology ; Drug Carriers/administration & dosage ; Female ; Histocytochemistry ; Ketamine/adverse effects ; Liposomes/administration & dosage ; Magnetic Resonance Imaging ; Orphan Drug Production ; Rats, Sprague-Dawley ; Treatment Outcome
    Chemical Substances Analgesics ; Anti-Inflammatory Agents ; Drug Carriers ; Liposomes ; Ketamine (690G0D6V8H) ; Botulinum Toxins, Type A (EC 3.4.24.69) ; onabotulinum toxin A (EC 3.4.24.69)
    Language English
    Publishing date 2018-04-11
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-018-24239-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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