Effects of Modified Zhisou Powder on Airway Mucus Production in Chronic Obstructive Pulmonary Disease Model Rats with Cold-Dryness Syndrome

Gao, Zhen; Wang, Jing; Jing, Jing; Xu, Dan; Zheng, Li; Li, Fengsen

doi:10.1155/2018/7297141

Cited by 8 publications

(4 citation statements)

References 34 publications

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“…In light of its time-effectiveness, this method is still being used by researchers to establish COPD animal models. Another available method is the one proposed by Zhen et al [20] who established the COPD model in 90 days, simply by exposing rats to Hataman cigarette smoke (two 1-h sessions of smoke exposure, per day) and infusing them with elastase (2 U kg − 1 body weight) on the 30th day. The model has also been set up by combining Klebsiella pneumonia dilution with incremental CSE [21].…”

Section: Establishment Of the Copd Skeletal Muscle Dysfunction Model mentioning

confidence: 99%

“…The reduced function and altered structure of lungs are considered to be important indicators of COPD [20,27]. In clinical pulmonary function tests, the specific manifestations of COPD p include decreased FEV1/FVC levels [28], as well as reduced expressions of MMEF and other ventilation indicators [29].…”

Section: Effect Of Incremental Smoke Exposure On Lung Function and Stmentioning

confidence: 99%

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The rat model of COPD skeletal muscle dysfunction induced by progressive cigarette smoke exposure: a pilot study

et al. 2020

BMC Pulm Med

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Background: Chronic obstructive pulmonary disease (COPD) skeletal muscle dysfunction is a prevalent malady that significantly affects patients' prognosis and quality of life. Although the study of this disease has attracted considerable attention, a definite animal model is yet to be established. This study investigates whether smoke exposure could lead to the development of a COPD skeletal muscle dysfunction model in rats. Methods: Sprague Dawley rats were randomly divided into model (MG, n = 8) and control groups (CG, n = 6). The MG was exposed to cigarette smoke for 16 weeks while the CG was not. The body weight and forelimb grip strength of rats were monitored monthly. The pulmonary function and the strength of tibialis anterior muscle were assessed in vitro and compared after establishing the model. The histological changes in lung and gastrocnemius muscles were observed. The expressions of interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α were detected by ELISA, while the expressions of Atrogin-1 and MuRF1 in the gastrocnemius muscle were determined by Western blotting. Results: Smoke exposure slowly increases the body weight and forelimb grip strength of MG rats, compared to CG rats. However, it significantly decreases the pulmonary ventilation function and the skeletal muscle contractility of the MG in vitro. Histologically, the lung tissues of MG show typical pathological manifestations of emphysema, while the skeletal muscles present muscular atrophy. The expressions of IL-6, IL-8, and TNF-α in MG rats are significantly higher than those measured in CG rats. Increased levels of Atrogin-1 and MuRF1 were also detected in the gastrocnemius muscle tissue of MG. Conclusion: Progressive smoking exposure decreases the contractile function of skeletal muscles, leading to muscular atrophy. It also increases the expressions of inflammatory and muscle protein degradation factors in COPD rats. This indicates that smoke exposure could be used to establish a COPD skeletal muscle dysfunction model in rats.

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Section: Establishment Of the Copd Skeletal Muscle Dysfunction Model mentioning

confidence: 99%

Section: Effect Of Incremental Smoke Exposure On Lung Function and Stmentioning

confidence: 99%

The rat model of COPD skeletal muscle dysfunction induced by progressive cigarette smoke exposure: a pilot study

et al. 2020

BMC Pulm Med

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“…The expression of AQPs and MUC5AC was significantly decreased when TNF- α secretion was increased. In addition, MUC5AC will be correspondingly decreased when AQPs expression level increases after treatment [ 35 ]. MUC5AC synthesis and secretion increased by 57.9% and 85.3%, respectively, after five days of AQPs gene knockout in airway glands [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

Gandan Oral Liquid Improves Exudative Pneumonia by Upregulating Bacteria Clearance via Regulating AQP5 and MUC5AC in Rats

Wang

Yan

Wang

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Gandan oral liquid (GOL) is a mixture of crude extracts from licorice and Radix isatidis. Clinically, it has been widely used in the treatment of exudative pneumonia (EP) in animals. But the molecular mechanism of these effects is unclear. Therefore, antibacterial activity and therapeutic effect were tested in vitro and in vivo. Exudative pneumonia was established with the intraperitoneal injection of LPS, followed by continuous intranasal inoculation of Klebsiella pneumoniae (KP). After that, Gandan oral liquid, acetylcysteine, and levofloxacin were given through the intragastric route for five days, and clinical symptoms were observed and counted. The bacterial content of alveolar lavage fluid was determined, hematology analysis was performed, and lung histology examination was performed. Western blotting, immunohistochemistry, and immunofluorescence were used to detect the expression levels of AQP3, AQP5, and MUC5AC in lung tissues. ELISA kit was used to detect serum and BALF cytokines levels. The results showed that GOL (242 mg/mL) had no antibacterial activity on Klebsiella pneumonia (KP), and the effect was significantly worse than levofloxacin. However, the therapeutic test in vivo of the rat model of bacterial EP showed different results. After treatment, GOL administration ameliorated EP and increased the expression of mucoprotein -5AC (MUC5AC), and GOL promoted water secretion of the respiratory tract by increasing the expression of aquaporin-5 (AQP5) and decreasing the levels of proinflammatory cytokines (TNF-α, IL-6, and IL-1β). Conclusion. GOL accelerates the water secretion of respiratory tract, inhibits the inflammatory response, induces removal of bacteria of respiratory tract via the AQPs/MUC pathway, and ultimately ameliorates EP.

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“…***: p < .001, compared with NC group; #: p < .05, ##: p < .01, ###: p < .001, compared with model group; $: p < .05, $$: p < .01, compared with low group; &: p < .05, compared with middle group activation of inflammatory cytokines in the airway, which is essential to induce inflammation, including TNFα, IL-1β, and IL-6. Numerous studies have found that the expression of TNFα, IL-1β, IL-6, and other inflammatory mediators significantly increased, with enhanced activities of caspase-3 and caspase-9, which might jointly result in damaged lung function and elevated number of apoptotic cells in lung tissue (Yamada et al, 2016;Zhen et al, 2018). In accordance with the results of our study, houttuynin treatment reduced the protein expression of caspase-3 and caspase-9 and downregulated the expression of inflammatory cytokines of TNFα, IL-1β, and IL-6.…”

Section: Discussionmentioning

confidence: 99%

Effect of houttuynia on improving lung injury in chronic obstructive pulmonary disease by regulating the TLR4 signaling pathway

Wang

et al. 2021

Food Science & Nutrition

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This study aimed to investigate the effects and mechanisms of houttuynia on lung pathological injury in rats with chronic obstructive pulmonary disease (COPD). Rats were randomly divided into the normal control, COPD model (model), low‐dose treatment (low, 5 mg/kg), middle‐dose treatment (middle, 10 mg/kg), and high‐dose treatment (high, 25 mg/kg) groups. The COPD rat model was induced by smoking combined with intratracheal instillation of lipopolysaccharide. The treatment groups were given Houttuynia by gavage at 30 min before smoking. The IL‐6, IL‐1β, and TNF‐α concentrations in serum and BALF were determined by ELISA. The pathological morphology was detected by HE staining. The apoptosis cell number was evaluated by TUNEL assay. Apoptotic proteins (caspase‐3 and caspase‐9) were measured by IHC assay in lung tissues. The relative proteins [TLR4, MyD88, and p‐NF‐κB(p65)] were evaluated by Western blot assay in lung tissues. Compared with the model group, the low, middle, and high groups could reduce pulmonary congestion, edema, inflammatory cell infiltration, and apoptosis cell number; downregulate the protein expression of caspase‐3, caspase‐9, TLR4, MyD88, and NF‐κB(p65) (p < .05); and inhibit the IL‐6, IL‐1β, and TNF‐α concentrations in serum and BALF. Houttuynia could improve the morphology and apoptosis cell number in lung tissues, thereby inhibiting the activation of the TLR4/MyD88/NF‐κB(p65) signaling pathway.

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Effects of Modified Zhisou Powder on Airway Mucus Production in Chronic Obstructive Pulmonary Disease Model Rats with Cold-Dryness Syndrome

Cited by 8 publications

References 34 publications

The rat model of COPD skeletal muscle dysfunction induced by progressive cigarette smoke exposure: a pilot study

The rat model of COPD skeletal muscle dysfunction induced by progressive cigarette smoke exposure: a pilot study

Gandan Oral Liquid Improves Exudative Pneumonia by Upregulating Bacteria Clearance via Regulating AQP5 and MUC5AC in Rats

Effect of houttuynia on improving lung injury in chronic obstructive pulmonary disease by regulating the TLR4 signaling pathway

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