Effect of DHU001, a Polyherbal Formula on Formalin-induced Paw Chronic Inflammation of Mice

Cho, Yoon-Hee; Chung, In-Kwon; Cheon, Woo-Hyun; Lee, Hyeung-Sik; Ku, Sae‐Kwang

doi:10.5487/tr.2011.27.2.095

Cited by 12 publications

(8 citation statements)

References 21 publications

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“…All of the intact vehicle control mice exhibited normal body weight gain throughout the experimental period, including during the 10 days of acclimation ( 80 , 81 ). The DEXA-induced decreases in body weight detected in the present study were considered to be related to cachexia, due to the potent catabolic effects of DEXA ( 82 , 83 ). Conversely, the increased body weight detected in mice treated with EAP may be associated with the known immunomodulatory effects of EAP ( 45 , 84 ).…”

Section: Discussionmentioning

confidence: 62%

Extracellular polysaccharides purified from Aureobasidium pullulans SM‑2001 (Polycan) inhibit dexamethasone‑induced muscle atrophy in mice

Lim¹,

Lee

Cho³

et al. 2017

Int J Mol Med

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Abstract. The present study assessed the beneficial skeletal muscle-preserving effects of extracellular polysaccharides from Aureobasidium pullulans SM-2001 (Polycan) (EAP) on dexamethasone (DEXA)-induced catabolic muscle atrophy in mice. To investigate whether EAP prevented catabolic DEXA-induced muscle atrophy, and to examine its mechanisms of action, EAP (100, 200 and 400 mg/kg) was administered orally, once a day for 24 days. EAP treatment was initiated 2 weeks prior to DEXA treatment (1 mg/kg, once a day for 10 days) in mice. Body weight alterations, serum biochemistry, calf thickness, calf muscle strength, gastrocnemius muscle thickness and weight, gastrocnemius muscle antioxidant defense parameters, gastrocnemius muscle mRNA expression, histology and histomorphometry were subsequently assessed. After 24 days, DEXA control mice exhibited muscle atrophy according to all criteria indices. However, these muscle atrophy symptoms were significantly inhibited by oral treatment with all three doses of EAP. Regarding possible mechanisms of action, EAP exhibited favorable ameliorating effects on DEXA-induced catabolic muscle atrophy via antioxidant and anti-inflammatory effects; these effects were mediated by modulation of the expression of genes involved in muscle protein synthesis (AKT serine/threonine kinase 1, phosphatidylinositol 3-kinase, adenosine A1 receptor and transient receptor potential cation channel subfamily V member 4) and degradation (atrogin-1, muscle RING-finger protein-1, myostatin and sirtuin 1). Therefore, these results indicated that EAP may be helpful in improving muscle atrophies of various etiologies. EAP at 400 mg/kg exhibited favorable muscle protective effects against DEXA-induced catabolic muscle atrophy, comparable with the effects of oxymetholone (50 mg/kg), which has been used to treat various muscle disorders.

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Section: Discussionmentioning

confidence: 62%

Extracellular polysaccharides purified from Aureobasidium pullulans SM‑2001 (Polycan) inhibit dexamethasone‑induced muscle atrophy in mice

Lim¹,

Lee

Cho³

et al. 2017

Int J Mol Med

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“…1 ). This decrease in body weight induced by treatment with dexamethasone was considered to be due to cachexia-related changes resulting from the potent catabolic effects of dexamethasone itself ( 51 , 52 ), and the increase in body weight detected with all 3 FS concentrations may be related at least in part to the well-documented immuno modulatory effects of FS ( 53 , 54 ). Generally, animals with enhanced immune systems show relatively good growth patterns ( 55 , 56 ).…”

Section: Discussionmentioning

confidence: 99%

The administration of Fructus Schisandrae attenuates dexamethasone-induced muscle atrophy in mice

Kim

Han

et al. 2015

International Journal of Molecular Medicine

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In the present study, we aimed to determine whether ethanol extracts of Fructus Schisandrae (FS), the dried fruit of Schizandra chinensis Baillon, mitigates the development of dexamethasone-induced muscle atrophy. Adult SPF/VAT outbred CrljOri:CD1 (ICR) mice were either treated with dexamethasone to induce muscle atrophy. Some mice were treated with various concentrations of FS or oxymetholone, a 17α-alkylated anabolic-androgenic steroid. Muscle thickness and weight, calf muscle strength, and serum creatine and creatine kinase (CK) levels were then measured. The administration of FS attenuated the decrease in calf thickness, gastrocnemius muscle thickness, muscle strength and weight, fiber diameter and serum lactate dehydrogenase levels in the gastrocnemius muscle bundles which was induced by dexamethasone in a dose-dependent manner. Treatment with FS also prevented the dexamethasone-induced increase in serum creatine and creatine kinase levels, histopathological muscle fiber microvacuolation and fibrosis, and the immunoreactivity of muscle fibers for nitrotyrosine, 4-hydroxynonenal, inducible nitric oxide synthase and myostatin. In addition, the destruction of the gastrocnemius antioxidant defense system was also inhibited by the administration of FS in a dose-dependent manner. FS downregulated the mRNA expression of atrogin-1 and muscle RING-finger protein-1 (involved in muscle protein degradation), myostatin (a potent negative regulator of muscle growth) and sirtuin 1 (a representative inhibitor of muscle regeneration), but upregulated the mRNA expression of phosphatidylinositol 3-kinase, Akt1, adenosine A1 receptor and transient receptor potential cation channel subfamily V member 4, involved in muscle growth and the activation of protein synthesis. The overall effects of treatment with 500 mg/kg FS were comparable to those observed following treatment with 50 mg/kg oxymetholone. The results from the present study support the hypothesis that FS has a favorable ameliorating effect on muscle atrophy induced by dexamethasone, by exerting anti-inflammatory and antioxidant effects on muscle fibers, which may be due to an increase in protein synthesis and a decrease in protein degradation.

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“…Animals in all groups were injected with 0.02 mL of 1% formalin in the right hind paw to produce chronic inflammation. 16,17 Group I animals were kept as control without any drug treatment. The animals in group II received standard reference drug diclofenac at 10 mg/kg body weight (bwt) intraperitoneally.…”

Section: Effect Of Vco On Formalin-induced Chronic Inflammationmentioning

confidence: 99%

Virgin coconut oil supplementation ameliorates cyclophosphamide-induced systemic toxicity in mice

et al. 2015

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Virgin coconut oil (VCO) is an unrefined kernal oil, prepared from Cocos nucifera L., having substantial nutritional and medicinal value. Experimental studies have suggested its antioxidant, anti-inflammatory, immunostimulatory and hypolipidemic effects. The present study assesses its effect on formalin-induced chronic inflammation and cyclophosphamide (CTX)-induced systemic toxicity in murine models. Oral administration of VCO effectively reduced formalin-induced paw oedema in mice with more or less similar efficacy as that of diclofenac. The CTX-induced hike in blood urea, creatinine, thiobarbituric acid reactive substances (TBARS) and liver marker enzymes in mice was marginally decreased by VCO (8 g/kg body weight) ingestion orally. The liver and kidney catalase, superoxide dismutase and glutathione peroxidase activities, together with cellular glutathione and TBARS levels, were found to be improved in these animals. Overall the study reveals the protective efficacy of VCO against secondary toxicity induced by CTX possibly through its antioxidant and anti-inflammatory properties.

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Effect of DHU001, a Polyherbal Formula on Formalin-induced Paw Chronic Inflammation of Mice

Cited by 12 publications

References 21 publications

Extracellular polysaccharides purified from Aureobasidium pullulans SM‑2001 (Polycan) inhibit dexamethasone‑induced muscle atrophy in mice

Extracellular polysaccharides purified from Aureobasidium pullulans SM‑2001 (Polycan) inhibit dexamethasone‑induced muscle atrophy in mice

The administration of Fructus Schisandrae attenuates dexamethasone-induced muscle atrophy in mice

Virgin coconut oil supplementation ameliorates cyclophosphamide-induced systemic toxicity in mice

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