Animal models: An essential tool to dissect the heterogeneity of chronic obstructive pulmonary disease

Jiang, Jingxian; Xu, Shuanglan; Chen, Zi; Liu, Weihua; Zhang, Liuchao; Li, Jianmin; Zhu, Zhou; Zhou, Lei

doi:10.2478/jtim-2023-0007

Cited by 7 publications

(6 citation statements)

References 58 publications

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“…( 2017 ) have reported that Crocin may protect against cerebral ischemia in elderly patients by maintaining the integrity of the blood‐brain barrier. In this study, the classical methods of the OFT test, Y‐maze test, and MWM test were exploited to evaluate the behavior ability of AD model animals (Brandeis et al., 1989 ; Jiang et al., 2023 ). Consistent with previous reports, the present study also found that Crocin notably improved the cognitive deficits of Aβ 25‐35 ‐induced AD mice.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, Zhang et al (2017) have reported that Crocin may protect against cerebral ischemia in elderly patients by maintaining the integrity of the blood-brain barrier. In this study, the classical methods of the OFT test, Y-maze test, and MWM test were exploited to evaluate the behavior ability of AD model animals (Brandeis et al, 1989;Jiang et al, 2023).…”

Section: Discussionmentioning

confidence: 99%

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Crocin ameliorates neuroinflammation and cognitive impairment in mice with Alzheimer's disease by activating PI3K/AKT pathway

Su,

Wang,

Shao

et al. 2024

Brain and Behavior

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BackgroundCrocin has a good prospect in the treatment of Alzheimer's disease (AD), but the mechanisms underlying its neuroprotective effects remain elusive. This study aimed to investigate the neuroprotective effects of Crocin and its underlying mechanisms in AD.MethodsAD mice were set up by injecting Aβ25‐35 solution into the hippocampus. Then, the AD mice were injected intraperitoneally with 40 mg/kg/day of Crocin for 14 days. Following the completion of Crocin treatment, an open‐field test, Y‐maze test and Morris water maze test were conducted to evaluate the impact of Crocin on spatial learning and memory deficiency in mice. The effects of Crocin on hippocampal neuron injury, proinflammatory cytokine expressions (IL‐1β, IL‐6, and TNF‐α), and PI3K/AKT signaling‐related protein expressions were measured using hematoxylin and eosin staining, Western blot, and quantitative real‐time polymerase chain reaction (qRT‐PCR) experiments, respectively.ResultsCrocin attenuated Aβ25‐35‐induced spatial learning and memory deficiency and hippocampal neuron injury. Furthermore, the Western blot and qRT‐PCR results showed that Crocin effectively suppressed inflammation and activated the PI3K/AKT pathway in Aβ25‐35‐induced mice.ConclusionCrocin restrained neuroinflammation via the activation of the PI3K/AKT pathway, thereby ameliorating the cognitive dysfunction of AD mice.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Crocin ameliorates neuroinflammation and cognitive impairment in mice with Alzheimer's disease by activating PI3K/AKT pathway

Su,

Wang,

Shao

et al. 2024

Brain and Behavior

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“…Moreover recent studies have found that EMT occurs in the small airway epithelium of patients with COPD [ 38 ], and may play an important role in the occurrence and development of airway remodelling. Smoking is one of the most important causes of COPD [ 39 ], and current studies have mainly focused on the effects of CS on the EMT in COPD. CS acts on EMT through various pathways, including oxidative stress, destruction of cell connections, and destruction of the cytoskeletal structure.…”

Section: Discussionmentioning

confidence: 99%

HDAC6-selective inhibitor CAY10603 ameliorates cigarette smoke-induced small airway remodeling by regulating epithelial barrier dysfunction and reversing

Zhang,

Yan,

et al. 2024

Respir Res

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Background Small airway remodelling is a vital characteristic of chronic obstructive pulmonary disease (COPD), which is mainly caused by epithelial barrier dysfunction and epithelial-mesenchymal transition (EMT). Recent studies have indicated that histone deacetylase 6 (HDAC6) plays an important role in the dysregulation of epithelial function. In this study, we investigated the therapeutic effects and underlying mechanisms of an inhibitor with high selectivity for HDAC6 in COPD. Methods Cigarette smoke (CS) exposure was used to establish a CS-induced COPD mouse model. CAY10603 at doses of 2.5 and 10 mg/kg was injected intraperitoneally on alternate days. The protective effects of CAY10603 against CS-induced emphysema, epithelial barrier function and small airway remodeling were evaluated using hematoxylin and eosin (H&E) staining, Masson’s trichrome staining, immunohistochemical staining, and western blot. The human lung bronchial epithelial cell line (HBE) was used to elucidate the underlying molecular mechanism of action of CAY10603. Results HDAC6 levels in the lung homogenates of CS-exposed mice were higher than that those in control mice. Compared to the CS group, the mean linear intercept (MLI) of the CAY10603 treatment group decreased and the mean alveolar number (MAN)increased. Collagen deposition was reduced in groups treated with CAY10603. The expression of α-SMA was markedly upregulated in the CS group, which was reversed by CAY10603 treatment. Conversely, E-cadherin expression in the CS group was further downregulated, which was reversed by CAY10603 treatment. CAY10603 affects the tight junction protein expression of ZO-1 and occludin. ZO-1 and occludin expression were markedly downregulated in the CS group. After CAY10603treatment, the protein expression level of ZO-1 and occludin increased significantly. In HBE cells, Cigarette smoke extract (CSE) increased HDAC6 levels. CAY10603 significantly attenuated the release of TGF-β1 induced by CSE. CAY10603 significantly increased the E-cadherin levels in TGF-β1 treated HBE cells, while concurrently attenuated α-SMA expression. This effect was achieved through the suppression of Smad2 and Smad3 phosphorylation. CAY10603 also inhibited TGF-β1 induced cell migration. Conclusions These findings suggested that CAY10603 inhibited CS induced small airway remodelling by regulating epithelial barrier dysfunction and reversing EMT via the TGF-β1/Smad2/3 signalling pathway.

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“…Guinea pigs develop many of the symptoms of human COPD, including emphysema, acute neutrophilia, increased epithelial permeability, and sustained monocyte recruitment after administration of CS or LPS [ 124 ]. Smoke and polyIC administration result in inflammatory responses similar to COPD exacerbations [ 93 ].…”

Section: Disease Modelsmentioning

confidence: 99%

Animals in Respiratory Research

Fröhlich

2024

IJMS

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The respiratory barrier, a thin epithelial barrier that separates the interior of the human body from the environment, is easily damaged by toxicants, and chronic respiratory diseases are common. It also allows the permeation of drugs for topical treatment. Animal experimentation is used to train medical technicians, evaluate toxicants, and develop inhaled formulations. Species differences in the architecture of the respiratory tract explain why some species are better at predicting human toxicity than others. Some species are useful as disease models. This review describes the anatomical differences between the human and mammalian lungs and lists the characteristics of currently used mammalian models for the most relevant chronic respiratory diseases (asthma, chronic obstructive pulmonary disease, cystic fibrosis, pulmonary hypertension, pulmonary fibrosis, and tuberculosis). The generation of animal models is not easy because they do not develop these diseases spontaneously. Mouse models are common, but other species are more appropriate for some diseases. Zebrafish and fruit flies can help study immunological aspects. It is expected that combinations of in silico, in vitro, and in vivo (mammalian and invertebrate) models will be used in the future for drug development.

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Animal models: An essential tool to dissect the heterogeneity of chronic obstructive pulmonary disease

Cited by 7 publications

References 58 publications

Crocin ameliorates neuroinflammation and cognitive impairment in mice with Alzheimer's disease by activating PI3K/AKT pathway

Crocin ameliorates neuroinflammation and cognitive impairment in mice with Alzheimer's disease by activating PI3K/AKT pathway

HDAC6-selective inhibitor CAY10603 ameliorates cigarette smoke-induced small airway remodeling by regulating epithelial barrier dysfunction and reversing

Animals in Respiratory Research

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