1. Metabolic Enzyme/Protease Anti-infection Immunology/Inflammation Apoptosis
  2. Renin Bacterial Interleukin Related TNF Receptor
  3. Theasinensin C

Theasinensin C is an orally effective renin inhibitor and gut microbiota modulator, with an IC50 of 40.21 μM against renin activity. Theasinensin C selectively enriches Akkermansia muciniphila in the gut microbiota, enhances the Akkermansia muciniphila-mediated hydrolysis of the PTS domain of mucin, drives the accumulation of luminal glutamine and serine, and regulates the gut-kidney-liver glutamine/serine metabolic signaling pathway to promote creatine biosynthesis. Theasinensin C improves cognitive function, reduces pro-inflammatory cytokines, alleviates neuropathological changes and restores intestinal barrier integrity. Theasinensin C can be used in research related to hypertension and neuroinflammation induced by high-fructose diet.

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Theasinensin C

Theasinensin C Chemical Structure

CAS No. : 89013-69-4

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Description

Theasinensin C is an orally effective renin inhibitor and gut microbiota modulator, with an IC50 of 40.21 μM against renin activity. Theasinensin C selectively enriches Akkermansia muciniphila in the gut microbiota, enhances the Akkermansia muciniphila-mediated hydrolysis of the PTS domain of mucin, drives the accumulation of luminal glutamine and serine, and regulates the gut-kidney-liver glutamine/serine metabolic signaling pathway to promote creatine biosynthesis. Theasinensin C improves cognitive function, reduces pro-inflammatory cytokines, alleviates neuropathological changes and restores intestinal barrier integrity. Theasinensin C can be used in research related to hypertension and neuroinflammation induced by high-fructose diet[1][2].

In Vitro

Theasinensin C (48 h) enhances Akkermansia muciniphila XJ 240720-mediated degradation of the mucin PTS domain, resulting in a significant increase in luminal L-glutamine and L-serine levels[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

Theasinensin C (150 mg/kg/day; oral gavage; daily; 8 weeks) mitigates HFrD-induced neuroinflammation in male C57BL/6J mice by improving cognitive function, reducing systemic and central inflammatory markers, restoring intestinal barrier integrity, and remodeling gut microbiota to enrich beneficial taxa like Akkermansia muciniphila[3].
Theasinensin C (150 mg/kg/day; oral gavage; daily; 8 weeks) attenuates HFrD-induced neuroinflammation in antibiotic-pretreated germ-free male C57BL/6J mice, with improvements in cognitive function and reduction of central inflammatory markers, though efficacy is enhanced when combined with Akkermansia muciniphila-derived metabolites[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6J (8-week-old male, SPF grade, HFrD-induced neuroinflammation)[3]
Dosage: 150 mg/kg/day
Administration: oral gavage; daily; 8 weeks
Result: Shortened escape latency in MWM training, increased percentage of distance and time spent in the target quadrant, and increased number of platform crossings compared to HFrD controls.
Decreased serum levels of LPS, TNF-α, and IL-6, and increased serum IL-10 levels compared to HFrD controls.
Reduced number of damaged neurons in the hippocampus and cortex; decreased mean fluorescence density of GFAP and IBA-1 in the hippocampus; downregulated hippocampal and cortical mRNA expression of Il-6, Tnf-α, Il-1β, Mcp-1, iNos, and Cox-2 compared to HFrD controls.
Alleviated colonic shortening, submucosal edema, inflammatory infiltration, crypt damage, and goblet cell loss; downregulated colonic mRNA expression of Tnf-α, Il-6, Il-1β, and Mcp-1; upregulated colonic mRNA expression of Zo-1, Occludin, Claudin-1, and Muc1 compared to HFrD controls.
Selectively enriched beneficial taxa; suppressed pro-inflammatory taxa including Desulfovibrio desulfuricans, Neisseria mucosa, Helicobacter hepaticus, and Ruminococcus gnavus compared to HFrD controls; restored HFrD-reduced levels of acetate, propionate, i-butyrate, n-butyrate, n-valerate, lactic acid, and total acids in colonic contents, and upregulated intestinal SCFA receptor genes Ffar2 and Ffar3.
Animal Model: C57BL/6J (8-week-old male, SPF grade, antibiotic-pretreated germ-free, HFrD-induced neuroinflammation)[3]
Dosage: 150 mg/kg/day
Administration: oral gavage; daily; 8 weeks
Result: Reduced escape latency in MWM training, increased percentage of distance and time spent in the target quadrant, and increased number of platform crossings compared to HFrD controls (efficacy was less than the combined metabolite group of theasinensin C and Akkermansia muciniphila, but greater than HFrD controls).
Reduced number of damaged neurons in the hippocampus and cortex; decreased mean fluorescence density of GFAP and IBA-1 in the hippocampus; downregulated hippocampal and cortical mRNA expression of Il-6, Tnf-α, Il-1β, Mcp-1, iNos, and Cox-2 compared to HFrD controls.
Molecular Weight

610.52

Formula

C30H26O14

CAS No.
SMILES

OC1=CC(O[C@@H]([C@@H](C2)O)C3=C(C4=C([C@H]5OC6=C(C[C@H]5O)C(O)=CC(O)=C6)C=C(O)C(O)=C4O)C(O)=C(O)C(O)=C3)=C2C(O)=C1

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Please store the product under the recommended conditions in the Certificate of Analysis.

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    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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Theasinensin C
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