ArticleActa pharmacologica Sinica2016
Cultured Mycelium Cordyceps sinensis allevi¬ates CCl4-induced liver inflammation and fibrosis in mice by activating hepatic natural killer cells.
Article in Acta pharmacologica Sinica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.
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20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.
- Efficacy of traditional Chinese medicineFrontiers in medicine · 2024Pooled it
- Efficacy and safety ofFrontiers in pharmacology · 2023Pooled it
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- Bicuculline fromComputational and structural biotechnology journal · 2026Article
- Metabolism of hepatic stellate cells in chronic liver diseases: emerging molecular and therapeutic interventions.Theranostics · 2025Review
- Immunopharmacological Insights intoCurrent pharmaceutical design · 2025Review
- Traditional Chinese Medicine,ACG case reports journal · 2023Article
- The Important Roles of Natural Killer Cells in Liver Fibrosis.Biomedicines · 2023Review
- The antifibrotic role of natural killer cells in liver fibrosis.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- Comparison of Widely Targeted Metabolomics and Untargeted Metabolomics of WildMolecules (Basel, Switzerland) · 2022Article
- Crosstalk between NK cells and hepatic stellate cells in liver fibrosis (Review).Molecular medicine reports · 2022Review
- Silibinin Schiff Base Derivatives Counteract CClDrug design, development and therapy · 2022Article
- Substantial involvement of TRPM7 inhibition in the therapeutic effect of Ophiocordyceps sinensis on pulmonary hypertension.Translational research : the journal of laboratory and clinical medicine · 2021Article
- The components data of fuzheng huayu extracts,Data in brief · 2019Article
- Tussah silkmoth pupae improve anti-tumor properties ofRSC advances · 2019Article
- Implications of immune-inflammatory responses in smooth muscle dysfunction and disease.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2019Article
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- IL-17 enhances oxidative stress in hepatocytes through Nrf2/keap1 signal pathway activation.International journal of clinical and experimental pathology · 2018Article
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- Lyn kinase enhanced hepatic fibrosis by modulating the activation of hepatic stellate cells.American journal of translational research · 2017Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
aimRecent evidence shows that cultured mycelium Cordyceps sinensis (CMCS) effectively protects against liver fibrosis in mice. Here, we investigated whether the anti-fibrotic action of CMCS was related to its regulation of the activity of hepatic natural killer (NK) cells in CCl4-treated mice.
methodsC57BL/6 mice were injected with 10% CCl4 (2 mL/kg, ip) 3 times per week for 4 weeks, and received CMCS (120 mg·kg(-1)·d(-1), ig) during this period. In another part of experiments, the mice were also injected with an NK cell-deleting antibody ASGM-1 (20 μg, ip) 5 times in the first 3 weeks. After the mice were sacrificed, serum liver function, and liver inflammation, hydroxyproline content and collagen deposition were assessed. The numbers of hepatic NK cells and expression of NKG2D (activation receptor of NK cells) on isolated liver lymphocytes were analyzed using flow cytometry. Desmin expression and cell apoptosis in liver tissues were studied using desmin staining and TUNEL assay, respectively. The levels of α-SMA, TGF-β, RAE-1δ and RAE-1ε in liver tissues were determined by RT-qPCR.
resultsIn CCl4-treated mice, CMCS administration significantly improved liver function, attenuated liver inflammation and fibrosis, and increased the numbers of hepatic NK cells and expression level of NKG2D on hepatic NK cells. Furthermore, CMCS administration significantly decreased desmin expression in liver tissues, and increased TUNEL staining adjacent to hepatic stellate cells. Injection with NK cell-deleting ASGM-1 not only diminished the numbers of hepatic NK cells, but also greatly accelerated liver inflammation and fibrosis in CCl4-treated mice. In CCl4-treated mice with NK cell depletion, CMCS administration decelerated the rate of liver fibrosis development, and mildly upregulated the numbers of hepatic NK cells but without changing NKG2D expression.
conclusionCMCS alleviates CCl4-induced liver inflammation and fibrosis via promoting activation of hepatic NK cells. CMCS partially reverses ASGM-1-induced depletion of hepatic NK cells.
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