Suppression of expression and/or plasm levels of cytokine IL-11, a member of the IL-6 cytokine family, slows aging in both male and female mice.
The study (https://pubmed.ncbi.nlm.nih.gov/39020175/) caught my attention, and I researched what herbals might produce such inhibition, because I’m not interested (at 86) in waiting for drugs to be developed with the usual numerous side effects. Herbal inhibitors of IL-11 are well documented, and here is a short list:
Key Herbal Inhibitors of IL-11
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Quercetin: This flavanol antioxidant found in many plant foods suppresses inflammation and fibrosis, and inhibits IL-11 activation by downregulating JAK/STAT signaling. Quercetin may exert effects through its antioxidant and anti-inflammatory properties, benefiting conditions linked to IL-11 overactivity.
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Resveratrol: Known for anti-inflammatory actions, resveratrol can suppress JAK/STAT pathway activation and partially inhibit IL-11, especially in gut and metabolic disease models.
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Curcumin: The principal curcuminoid in turmeric, curcumin inhibits JAK1/2 and STAT3 signaling and has anti-inflammatory properties that extend to IL-11 suppression as part of its broader cytokine modulation.
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Apigenin and Luteolin: Flavonoids with strong JAK/STAT pathway inhibition, reducing IL-11-induced effects. Luteolin is noted for its cell-protective and inflammation-modulating activities.
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Omega-3 Polyunsaturated Fatty Acids (PUFAs): Found in marine oils, omega-3s directly suppress IL-11 production and subsequent ERK1/2-STAT3 signaling in hepatocytes and other models, especially during tissue injury.
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Osthole (from Cnidium monnieri): Shown to directly inhibit the IL-11/ERK1/2 axis, reducing fibrotic protein translation in renal fibrosis and alleviating disease progression.
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Mulberry leaf extract: Through inhibition of the NADPH oxidase/ROS/ERK axis, it can indirectly suppress IL-11 and its pro-fibrotic effects in diabetes models.
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Scutellaria baicalensis (Baicalin): Included in traditional combinations, this herb, and its flavonoids may decrease IL-11 and related pro-fibrotic signaling in animal models. It also increases Klotho expression and thereby healthspan.
Of this list, there are only two that I am not taking full time; Osthole and Mulberry Leaf Extract. The primary impacts of IL-11 are:
IL-11 is a key driver of fibrosis, inflammation, organ dysfunction, and several age-related and autoimmune pathologies.
Major Impacts of Elevated IL-11
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Multi-organ Fibrosis: IL-11 powerfully activates myofibroblast differentiation via ERK, causing extracellular matrix production and tissue fibrosis in the heart, liver, lung, kidney, pancreas, and vasculature. Its fibrogenic effects occur downstream of TGFβ1, often amplifying “canonical” fibrosis signals and contributing to organ failure.
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Impaired Tissue Regeneration: In the lung, kidney, and liver, IL-11 blocks normal epithelial or parenchymal cell repair by driving partial EMT (Epithelial–Mesenchymal Transition) and sustaining a dysfunctional progenitor state, promoting chronic degeneration instead of regeneration.
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Cardiac Dysfunction and Arrhythmia: IL-11 directly impairs contractility of cardiomyocytes, and its excess induces cardiac inflammation, fibrosis, arrhythmias (notably atrial fibrillation), and heart failure.
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Autoimmune and Inflammatory Diseases: High IL-11 is linked to rheumatoid arthritis, particularly in active disease and RA-associated interstitial lung disease, driving synovial and vascular inflammation, neoangiogenesis, and tissue damage.
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Renal Failure: In kidney disease, IL-11 causes tubular epithelial cell dysfunction, partial EMT, and promotes chronic inflammation, leading to progressive renal fibrosis and failure.
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Pulmonary Disorders: IL-11 impairs alveolar repair and drives fibrosis in idiopathic pulmonary fibrosis, HPS, and may contribute to other lung diseases marked by chronic inflammation or EMT.
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Inflammaging and Cancer Risk: Chronic IL-11 elevation fuels sterile inflammation (“inflammaging”), increasing risk of cancer, atherosclerosis, and autoimmune disorders.
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Vascular Disease: IL-11 enhances vascular smooth muscle cell dedifferentiation and vascular fibrosis, worsening restenosis after injury and promoting atherosclerotic changes.
Cellular and Systemic Pathologies
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IL-11 drives multiple mesenchymal transitions (EMT, EndoMT, FMT, VMT), contributing to cellular senescence, migration, and invasion in disease contexts.
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It plays roles in rare genetic syndromes (e.g., Peutz-Jeghers, Marfan, Alport, Loeys–Dietz), often via amplifying canonical pro-fibrotic signals.
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It is a master regulator of fibroblast, vascular, immune, and epithelial dysfunction, making it a high-value therapeutic target for disorders marked by chronic fibrosis, failed tissue repair, and excessive inflammation.
IL-11’s detrimental impacts span chronic fibrosis, organ failure, autoimmune activation, impaired repair, induction of cellular senescence, and inflammaging/cancer risk, making it central to the pathology of many widespread and rare diseases.
Sounds like a good thing to suppress and inhibit as we age!
To Your Greater Health and Fitness,
Frank
Frank Wilhelmi - Retired/consultant electronic engineer researches and reports practical strategies for optimizing health and fitness into advanced age. “I have a passion for living life to the fullest, and helping others to do the same.” A rapidly growing body of knowledge now enables us to extend our health and fitness decades beyond popular expectations.