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Article: Gut-liver axis modulation of Panax notoginseng saponins in nonalcoholic fatty liver disease
Title | Gut-liver axis modulation of Panax notoginseng saponins in nonalcoholic fatty liver disease |
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Authors | |
Keywords | PNS NAFLD Steatosis Fibrosis Leaky gut |
Issue Date | 2021 |
Publisher | Springer (India) Private Ltd. The Journal's web site is located at http://www.springer.com/medicine/internal/journal/12072 |
Citation | Hepatology International, 2021, v. 15, p. 350-365 How to Cite? |
Abstract | Background and aims:
Nonalcoholic fatty liver disease (NAFLD) is an obesity-related comorbidity, and it is characterized as a spectrum of liver abnormalities, including inflammation, steatosis, and fibrosis. The gut-liver axis is implicated in the pathogenesis and development of NAFLD. A promising drug agent targeting the gut-liver axis is expected to reverse NAFLD.
Methods:
We utilized high-fat diet (HFD)-induced obese mice and obesity-prone Lepob mice to examine the gut-liver regulation of the natural medicine Panax Notoginseng Saponins (PNS) on NAFLD.
Results:
PNS exhibited potent anti-lipogenesis and anti-fibrotic effects in NAFLD mice, that was associated with the TLR4-induced inflammatory signalling pathway in liver. More strikingly, PNS treatment caused a deceleration of gut-to-liver translocation of microbiota-derived short chain fatty acids (SCFAs) products. PNS-induced TLR4 inhibition and restoration of Claudin-1 and ZO-1 proteins in the gut-liver axis contributed to the reverse of leaky gut, which in turn abolished by the addition of lipopolysaccharide (LPS), an agonist of TLR4. Specifically, hepatic steatosis in HFD-treated mice was attenuated by PNS through regulating AMPKα, but restored by the replenishment of LPS. Meanwhile, the anti-fibrotic effect of PNS was abolished by LPS stimulation via the overproduction of collagen I/IV and α-SMA.
Conclusion:
PNS exerted hepatoprotection against NAFLD in both ob/ob and HFD-induced obese mice, primarily by mediating the gut-liver axis in a TLR4-dependent manner. |
Description | Hybrid open access |
Persistent Identifier | http://hdl.handle.net/10722/297609 |
ISSN | 2023 Impact Factor: 5.9 2023 SCImago Journal Rankings: 1.813 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Xu, Y | - |
dc.contributor.author | Wang, N | - |
dc.contributor.author | Tan, HY | - |
dc.contributor.author | Li, S | - |
dc.contributor.author | ZHANG, C | - |
dc.contributor.author | Feng, Y | - |
dc.date.accessioned | 2021-03-23T04:19:23Z | - |
dc.date.available | 2021-03-23T04:19:23Z | - |
dc.date.issued | 2021 | - |
dc.identifier.citation | Hepatology International, 2021, v. 15, p. 350-365 | - |
dc.identifier.issn | 1936-0533 | - |
dc.identifier.uri | http://hdl.handle.net/10722/297609 | - |
dc.description | Hybrid open access | - |
dc.description.abstract | Background and aims: Nonalcoholic fatty liver disease (NAFLD) is an obesity-related comorbidity, and it is characterized as a spectrum of liver abnormalities, including inflammation, steatosis, and fibrosis. The gut-liver axis is implicated in the pathogenesis and development of NAFLD. A promising drug agent targeting the gut-liver axis is expected to reverse NAFLD. Methods: We utilized high-fat diet (HFD)-induced obese mice and obesity-prone Lepob mice to examine the gut-liver regulation of the natural medicine Panax Notoginseng Saponins (PNS) on NAFLD. Results: PNS exhibited potent anti-lipogenesis and anti-fibrotic effects in NAFLD mice, that was associated with the TLR4-induced inflammatory signalling pathway in liver. More strikingly, PNS treatment caused a deceleration of gut-to-liver translocation of microbiota-derived short chain fatty acids (SCFAs) products. PNS-induced TLR4 inhibition and restoration of Claudin-1 and ZO-1 proteins in the gut-liver axis contributed to the reverse of leaky gut, which in turn abolished by the addition of lipopolysaccharide (LPS), an agonist of TLR4. Specifically, hepatic steatosis in HFD-treated mice was attenuated by PNS through regulating AMPKα, but restored by the replenishment of LPS. Meanwhile, the anti-fibrotic effect of PNS was abolished by LPS stimulation via the overproduction of collagen I/IV and α-SMA. Conclusion: PNS exerted hepatoprotection against NAFLD in both ob/ob and HFD-induced obese mice, primarily by mediating the gut-liver axis in a TLR4-dependent manner. | - |
dc.language | eng | - |
dc.publisher | Springer (India) Private Ltd. The Journal's web site is located at http://www.springer.com/medicine/internal/journal/12072 | - |
dc.relation.ispartof | Hepatology International | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject | PNS | - |
dc.subject | NAFLD | - |
dc.subject | Steatosis | - |
dc.subject | Fibrosis | - |
dc.subject | Leaky gut | - |
dc.title | Gut-liver axis modulation of Panax notoginseng saponins in nonalcoholic fatty liver disease | - |
dc.type | Article | - |
dc.identifier.email | Xu, Y: xyzjh@hku.hk | - |
dc.identifier.email | Wang, N: ckwang@hku.hk | - |
dc.identifier.email | Tan, HY: hyhtan@HKUCC-COM.hku.hk | - |
dc.identifier.email | Li, S: lishaha@HKUCC-COM.hku.hk | - |
dc.identifier.email | Feng, Y: yfeng@hku.hk | - |
dc.identifier.authority | Wang, N=rp02075 | - |
dc.identifier.authority | Feng, Y=rp00466 | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1007/s12072-021-10138-1 | - |
dc.identifier.pmid | 33656663 | - |
dc.identifier.pmcid | PMC8144126 | - |
dc.identifier.scopus | eid_2-s2.0-85102073817 | - |
dc.identifier.hkuros | 321786 | - |
dc.identifier.volume | 15 | - |
dc.identifier.spage | 350 | - |
dc.identifier.epage | 365 | - |
dc.identifier.isi | WOS:000625067900001 | - |
dc.publisher.place | India | - |