Therapeutic Potential of Traditional Chinese Medicine on Inflammatory Diseases

Tsai, Wen Hsin; Yang, Chi‐Rei; Li, Ping Chia; Chen, Wang Chuan; Chien, Chiang Ting

doi:10.4103/2225-4110.114898

Cited by 45 publications

(32 citation statements)

References 74 publications

(154 reference statements)

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“…33 Recent notions suggest a detrimental role for autophagy in toxin-mediated and ischemia/reperfusion-induced acute tissue injury. 33 The inhibition of LC3 II-mediated autophagy may be a new target for therapeutic exploration. One herbal medication that has gained recent popularity is the component L-theanine existing in a popular beverage of green tea.…”

Section: Discussionmentioning

confidence: 99%

l‐Theanine inhibits proinflammatory PKC/ERK/ICAM‐1/IL‐33 signaling, apoptosis, and autophagy formation in substance P‐induced hyperactive bladder in rats

Tsai

et al. 2016

Neurourology and Urodynamics

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Section: Discussionmentioning

confidence: 99%

l‐Theanine inhibits proinflammatory PKC/ERK/ICAM‐1/IL‐33 signaling, apoptosis, and autophagy formation in substance P‐induced hyperactive bladder in rats

Tsai

et al. 2016

Neurourology and Urodynamics

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“…Adenosine is a potent endogenous regulator of inflammation and tissue repair. Adenosine, which might be released from injured and hypoxic tissue in response to toxins and medications, may induce hepatic fibrosis in mice, presumably via adenosine receptor [ 42 – 44 ].

Fig.…”

Section: Discussionmentioning

confidence: 99%

Pre-administration of turmeric prevents methotrexate-induced liver toxicity and oxidative stress

Moghadam

Tutunchi

Namvaran-Abbas-Abad

et al. 2015

BMC Complement Altern Med

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BackgroundMethotrexate (MTX) is an antimetabolite broadly used in treatment of cancer and autoimmune diseases. MTX-induced hepatotoxicity limits its application. We investigated hepatoprotective effects of turmeric in MTX-induced liver toxicity.MethodsAll experiments were performed on male Wistar albino rats that were randomly divided into six groups. Group one received saline orally for 30 days (control group), groups two and three received turmeric extract (100, 200 mg/kg respectively) orally for 30 days, group four received single dose, of MTX IP at day 30, groups five and six received turmeric extract 100 and 200 mg/kg orally respectively for 30 days and single dose of methoterxate IP (20 mg/kg) at day 30. Four days after MTX injection animals were sacrificed and evaluated. Blood ALT and AST (indicators of hepatocyte injury), ALP and bilirubin (markers of biliary function), albumin (reflect liver synthetic function) as well as the plasma TAS concentration (antioxidant defenses) were determined. The cellular antioxidant defense activities were examined in liver tissue samples using SOD, CAT, and GSH-Px for the oxidative stress, and MDA for lipid peroxidation. In addition, liver damage was evaluated histopathologically.ResultsMTX significantly induced liver damage (P < 0.05) and decreased its antioxidant capacity, while turmeric was hepatoprotective. Liver tissue microscopic evaluation showed that MTX treatment induced severe centrilobular and periportal degeneration, hyperemia of portal vein, increased artery inflammatory cells infiltration and necrosis, while all of histopathological changes were attenuated by turmeric (200 mg/kg).ConclusionTurmeric extract can successfully attenuate MTX-hepatotoxicity. The effect is partly mediated through extract’s antinflammatory activity.

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“…Increased oxidative stress induces inflammation to several tissues/organs leading to cell death and long‐term injury. TCM with antioxidant, anti‐inflammatory, anti‐apoptotic, and autophagic regulatory functions has been widely used as preventive or therapeutic strategy in modern medicine . Oxidative stress and inflammation have been widely reported to contribute to SP‐mediated neurogenic hyperactive bladder .…”

Section: Discussionmentioning

confidence: 99%

Ba-Wei-Di-Huang-Wan through its active ingredient loganin counteracts substance P-enhanced NF-κB/ICAM-1 signaling in rats with bladder hyperactivity

Tsai

Cheng

et al. 2015

Neurourol. Urodynam.

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Overt bladder afferent activation may exacerbate endogenous substance P (SP) release to induce intercellular adhesion molecule-1 (ICAM-1)-mediated inflammation and reactive oxygen species (ROS) production leading to hyperactive bladder. Ba-Wei-Die-Huang-Wan (BWDHW), a traditional Chinese medicine, has been used to treat lower urinary tract symptoms in patients by undefined mechanisms. We explored the possible mechanisms and the active components of BWDHW on exogenous SP-induced bladder hyperactivity. BWDHW contained six major components: loganin, paeoniflorin, 5-hydroxymethylfurfural, cinnamic acid, cinnamaldehyde, and paeonol by high-performance liquid chromatography. In urethane-anesthetized female Wistar rats, we evaluated transcystometrogram, pelvic afferent nerve activity by electrophysiologic recording techniques, ICAM-1 expression by Western blot and immunohistochemistry, ROS amount by an ultrasensitive chemiluminescence method and possible ROS sources from the different leukocytes by specific stains in SP-treated bladder. BWDHW and its major component loganin dose-dependently inhibited H2 O2 and HOCl activity in vitro. Intragastrical BWDHW (250 mg/kg) and loganin (5 mg/kg) twice daily for 2 weeks did not affect the baseline micturition parameters. Intra-arterial SP (20 µg/rat) through neurokinin-1 receptor activation increased voiding frequency (shortened intercontraction intervals), pelvic afferent nerve activity, bladder NF-κB/ICAM-1 expression, bladder ROS amount, neutrophils adhesion to venous endothelium, CD68 (monocyte/macrophage), and mast cell infiltration in the inflamed bladder. BWDHW and loganin pretreatment significantly depressed SP-enhanced pelvic afferent nerve activity, bladder NF-κB/ICAM-1 expression, leukocyte infiltration, and ROS amount, and subsequently improved bladder hyperactivity. In conclusion, our results suggest that BWDHW and its active component loganin improves bladder hyperactivity via inhibiting SP/neurokinin-1 receptor signaling and depressing NF-κB/ICAM-1 mediated oxidative injury and inflammation. Neurourol. Urodynam. 35:771-779, 2016. © 2015 Wiley Periodicals, Inc.

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Therapeutic Potential of Traditional Chinese Medicine on Inflammatory Diseases

Cited by 45 publications

References 74 publications

l‐Theanine inhibits proinflammatory PKC/ERK/ICAM‐1/IL‐33 signaling, apoptosis, and autophagy formation in substance P‐induced hyperactive bladder in rats

l‐Theanine inhibits proinflammatory PKC/ERK/ICAM‐1/IL‐33 signaling, apoptosis, and autophagy formation in substance P‐induced hyperactive bladder in rats

Pre-administration of turmeric prevents methotrexate-induced liver toxicity and oxidative stress

Ba-Wei-Di-Huang-Wan through its active ingredient loganin counteracts substance P-enhanced NF-κB/ICAM-1 signaling in rats with bladder hyperactivity

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