# Tea Polysaccharides Ameliorates Non-Alcoholic Fatty Liver Disease in Mice via Regulating Macrophages Polarization by Gut Microbial Metabolites

**Authors:** Daixin Liu, Ang Li, Ping Li

PMC · DOI: 10.3390/cimb48030338 · 2026-03-23

## TL;DR

Tea polysaccharides help reduce fatty liver disease in mice by changing gut microbes to reduce liver inflammation.

## Contribution

This study reveals that tea polysaccharides ameliorate NAFLD by modulating gut microbiota to promote anti-inflammatory macrophage polarization.

## Key findings

- Tea polysaccharides significantly reduce liver injury and inflammation in NAFLD mice.
- Tea polysaccharides promote M2 macrophage polarization in the liver.
- Tea polysaccharides enhance butyric acid production by gut microbiota, which indirectly regulates macrophage polarization.

## Abstract

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease and a global public health concern, for which there is currently no effective method to inhibit its progression. The pathogenesis of NAFLD is related to hepatic lipid metabolism disorders and liver inflammation. Previous studies have shown that tea polysaccharides (TPS) have the ability to regulate lipid metabolism and control inflammation. This study aimed to observe the effect of TPS on ameliorating NAFLD in a mouse model and to reveal its underlying mechanisms. In the current study, male C57BL/6J mice were fed a high-fat diet and administered 100 mg/kg TPS daily by gavage for 14 weeks. Then, liver injury indicators and macrophage polarization markers were detected. The results revealed that TPS could significantly ameliorate the progression of NAFLD and decrease liver injury indicators. Moreover, we found that treatment of NAFLD model mice with TPS could skew liver macrophages polarization from M1 to M2 type, which inhibited pro-inflammatory cytokines production and liver inflammation. Mechanistically, TPS cannot directly regulate the polarization of liver macrophages, but instead promotes the production of butyric acid by gut microbiota, which in turn regulates macrophage polarization. These findings suggest that TPS ameliorates NAFLD-associated inflammation by modulating the gut–liver axis and promoting M2 macrophage polarization, laying the foundation for the potential of TPS in the development of health foods for NAFLD.

## Linked entities

- **Chemicals:** butyric acid (PubChem CID 264)
- **Diseases:** non-alcoholic fatty liver disease (MONDO:0013209), NAFLD (MONDO:0013209)

## Full-text entities

- **Genes:** Il1b (interleukin 1 beta) [NCBI Gene 16176] {aka IL-1beta, Il-1b}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, Gpt (glutamic pyruvic transaminase, soluble) [NCBI Gene 76282] {aka 1300007J06Rik, 2310022B03Rik, ALT, ALT1, Gpt-1, Gpt1}, OCLN (occludin) [NCBI Gene 100506658] {aka BLCPMG, PPP1R115, PTORCH1}, Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}, Mrc1 (mannose receptor, C type 1) [NCBI Gene 17533] {aka CD206, MR}, HDAC9 (histone deacetylase 9) [NCBI Gene 9734] {aka HD7, HD7b, HD9, HDAC, HDAC7B, HDAC9B}, Slc17a5 (solute carrier family 17 (anion/sugar transporter), member 5) [NCBI Gene 235504] {aka 4631416G20Rik, 4732491M05, AST, ISSD, NSD, SD}, TJP1 (tight junction protein 1) [NCBI Gene 7082] {aka ZO-1}, Nfkb1 (nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105) [NCBI Gene 18033] {aka NF-KB1, NF-kappaB, NF-kappaB1, p105, p50, p50/p105}, Il18 (interleukin 18) [NCBI Gene 16173] {aka Igif, Il-18}, Adgre1 (adhesion G protein-coupled receptor E1) [NCBI Gene 13733] {aka DD7A5-7, EGF-TM7, Emr1, F4/80, Gpf480, Ly71}, Hcar2 (hydroxycarboxylic acid receptor 2) [NCBI Gene 80885] {aka Gpr109a, Gpr109b, HM74, Niacr1, PUMA-G, Pumag}, Nlrp3 (NLR family, pyrin domain containing 3) [NCBI Gene 216799] {aka AGTAVPRL, AII/AVP, Cias1, FCAS, FCU, MWS}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, TLR4 (toll like receptor 4) [NCBI Gene 7099] {aka ARMD10, CD284, TLR-4, TOLL}, Ffar2 (free fatty acid receptor 2) [NCBI Gene 233079] {aka GPCR43, Gpr43}, Tlr4 (toll-like receptor 4) [NCBI Gene 21898] {aka Lps, Ly87, Ran/M1, Rasl2-8}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, Nos2 (nitric oxide synthase 2, inducible) [NCBI Gene 18126] {aka MAC-NOS, NOS-II, Nos-2, Nos2a, i-NOS, iNOS}, Il10 (interleukin 10) [NCBI Gene 16153] {aka CSIF, If2a, Il-10}, Ffar3 (free fatty acid receptor 3) [NCBI Gene 233080] {aka Gm478, Gpr41}, Gapdh (glyceraldehyde-3-phosphate dehydrogenase) [NCBI Gene 14433] {aka Gapd}, Ccr2 (C-C motif chemokine receptor 2) [NCBI Gene 12772] {aka Cc-ckr-2, Ccr2a, Ccr2b, Ckr2, Ckr2a, Ckr2b}
- **Diseases:** insulin resistance (MESH:D007333), injury to (MESH:D014947), NAFLD (MESH:D065626), obesity (MESH:D009765), hepatic lipid metabolism disorders (MESH:D052439), weight gain (MESH:D015430), metabolic disorders (MESH:D008659), liver damage (MESH:D056486), fibrosis (MESH:D005355), liver injury (MESH:D017093), colitis (MESH:D003092), liver disease (MESH:D008107), hyperglycemia (MESH:D006943), liver lipid (MESH:D011017), MAFLD (MESH:D005234), hepatic inflammation (MESH:D007249)
- **Chemicals:** C010-2-1 (-), TG (MESH:D013866), streptomycin (MESH:D013307), trifluoroacetic acid (MESH:D014269), galacturonic acid (MESH:C007819), SYBR Green (MESH:C098022), chloroform (MESH:D002725), ethanol (MESH:D000431), fatty acids (MESH:D005227), Percoll (MESH:C016039), lactate (MESH:D019344), acetone (MESH:D000096), acetic acid (MESH:D019342), 1-phenyl-3-methyl-5-pyrazolone (MESH:D000077553), neomycin (MESH:D009355), monosaccharide (MESH:D009005), MDA (MESH:D015104), paraformaldehyde (MESH:C003043), ampicillin (MESH:D000667), arabinose (MESH:D001089), Butyric Acid (MESH:D020148), NaOH (MESH:D012972), propionic acid (MESH:C029658), sulfuric acid (MESH:C033158), Polysaccharides (MESH:D011134), lipid (MESH:D008055), galactose (MESH:D005690), Fat (MESH:D005223), Trizol (MESH:C411644), propionate (MESH:D011422), isobutyrate (MESH:D058610), Oil Red O (MESH:C011049), paraffin (MESH:D010232), metronidazole (MESH:D008795), formalin (MESH:D005557), acetonitrile (MESH:C032159), phenol (MESH:D019800), PBS (MESH:D007854), vancomycin (MESH:D014640), ortho-phosphoric acid (MESH:C030242), H&amp;E (MESH:D006371), penicillin (MESH:D010406), methanol (MESH:D000432), drinking water (MESH:D060766), LPS (MESH:D008070), DSS (MESH:D016264), HCl (MESH:D006851), Clodronate (MESH:D004002), TC (MESH:D013667), n-butanol (MESH:D020001), Acetate (MESH:D000085), saline (MESH:D012965), butyrate (MESH:D002087), 4-methylvaleric acid (MESH:C034527), SCFA (MESH:D005232), water (MESH:D014867), free fatty acids (MESH:D005230), isopropanol (MESH:D019840)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606], Faecalibacterium prausnitzii (species) [taxon 853], Camellia sinensis (black tea, species) [taxon 4442]
- **Cell lines:** /6J — Homo sapiens (Human), Cutaneous melanoma, Cancer cell line (CVCL_W797), C57BL/6J — Mus musculus (Mouse), Transformed cell line (CVCL_C0MW)

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13025315/full.md

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Source: https://tomesphere.com/paper/PMC13025315