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Outline
To observe the effect and mechanism of Celastrol extract on the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB) signaling pathway mediated by phosphatase and tensin homolog (PTEN) in idiopathic pulmonary fibrosis (IPF) model mice.
C57BL/6 mice were randomly divided into 4 groups with an average of 10 mice in each group, including normal group, model group, celastrol (1 mg·kg-1·d-1) group and pirfenidone (50 mg·kg-1·d-1) group. The IPF mouse model was established by intratracheal instillation of bleomycin (BLM). After successful modeling, each observation group was orally administered (ig), while the normal group was orally administered an equal amount of physiological saline for 28 consecutive days. The samples were taken out on the second day after the last administration. The pathological changes in lung tissue were observed through routine HE staining and collagen deposition in mouse lung interstitium and peribronchial tissue were observed through Masson special staining. Immunohistochemistry (IHC) method was used to detect the in situ expressions of PTEN and type I collagen in lung tissue, while quantitative real-time PCR (qRT-PCR)) was used to detect the mRNA expressions of PTEN, PI3K, PKB and interleukin (IL)-17β in lung tissue.
Compared with that of the normal group, the expression of type I collagen in the lung interstitium was significantly increased in the model group (P<0.05). The expressions of PI3K, PKB and IL-17β mRNA in lung tissue were significantly increased (P<0.05), and the expression of PTEN mRNA was significantly decreased (P<0.05). Compared with the model group, the celastrol and pirfenidone groups had a significant reduction in the expression of type I collagen in the lung tissue (P<0.05) and the expression of PTEN protein was significantly enhanced (P<0.05). The expressions of PI3K, PKB and IL-17β mRNA in lung tissue were significantly decreased (P<0.05), and the expression of PTEN mRNA was significantly increased (P<0.05).
Celastrol extract can effectively inhibit the structural damage of lung interstitium and alleviate pulmonary fibrosis. The mechanism may be achieved by activating PTEN and coordinating the inhibition of PI3K/PKB expression, reducing inflammatory response and preventing the deposition of pulmonary interstitial collagen.
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| 科 Family | 属数 Number of genus | 种数 Number of species | 占总种数比例 Percentage of total species (%) | 属 Genus | 种数 Number of species | 占总种数比例 Percentage of total species (%) |
|---|---|---|---|---|---|---|
| 鹅膏菌科Amanitaceae | 2 | 11 | 5.26 | 鹅膏菌属 Amanita | 10 | 4.78 |
| 小菇科 Mycenaceae | 2 | 12 | 5.74 | 丝盖伞属 Inocybe | 5 | 2.39 |
| 多孔菌科 Polyporaceae | 8 | 14 | 6.70 | 蜡蘑属 Laccaria | 5 | 2.39 |
| 红菇科 Russulaceae | 3 | 23 | 11.00 | 小皮伞属 Marasmius | 6 | 2.87 |
| 小菇属 Mycena | 11 | 5.26 | ||||
| 光柄菇属 Pluteus | 5 | 2.39 | ||||
| 红菇属 Russula | 17 | 8.13 | ||||
| 栓菌属 Trametes | 5 | 2.39 |
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