Ivermectin's Anti-Inflammatory Effects: The Research

Ivermectin is a medicine against parasites, a derivative of avermectin used against parasitic infections for about 50 years [1]. Reviews also describe an anti-inflammatory side: a 2016 review calls it “a broad-spectrum anti-parasitic drug with significant anti-inflammatory properties” [2], and a 2024 review links its blocking of nuclear factor kappa B (NF-kappa-B), a switch inside cells that turns on inflammatory signals, to its anti-inflammatory role in rosacea [1].

This page gathers the research behind that reputation. Many readers arrive from the page on ivermectin and gum disease, because gum disease is an inflammatory disease. Each finding is labelled by where it was found: in people, in mice, in rats, in fish, in cells in the laboratory, or in a cell-free test. Most findings come from animals and cells; the studies in people tested ivermectin cream on the skin, mainly in rosacea. Studies that found the opposite effect are reported too.

Table of Contents

  1. Why Researchers Study Ivermectin and Inflammation
  2. The Bacterial-Toxin Studies in Mice
  3. Studies in Immune Cells
  4. The NF-kappa-B Pathway
  5. Allergic Inflammation in the Airways and Skin
  6. Rosacea: Anti-Inflammatory Action in Human Skin
  7. P2X4 Receptors and Bacterial Killing
  8. Related Avermectins
  9. What Has Been Tested in People
  10. Inflammation of the Gums
  11. Key Research Papers
  12. Connections
  13. Featured Videos

Why Researchers Study Ivermectin and Inflammation

Inflammation is the body’s response to injury and infection: redness, swelling, heat and pain. Immune cells drive it with signalling proteins called cytokines, among them tumour necrosis factor alpha (TNF-alpha), interleukin 1 beta (IL-1 beta) and interleukin 6 (IL-6). It clears infection, but when too strong or too long it damages tissue; the site’s inflammation animation shows the cascade.

Ivermectin was discovered in the 1970s by Satoshi Ōmura and William C. Campbell; against parasites it acts on glutamate-gated chloride channels, found in invertebrates such as worms and insects [1]. The reviews describe a second side:

Many studies below use lipopolysaccharide (LPS), a molecule from the outer wall of Gram-negative bacteria, to start inflammation on demand in animals or cells, then test whether a drug calms it.

The Bacterial-Toxin Studies in Mice

In a 2008 study in mice, ivermectin or salt water was given by mouth, and the mice were then injected in the belly with a lethal dose of lipopolysaccharide (32 mg/kg) [6]. The findings:

The authors concluded that ivermectin “may inhibit LPS-induced production of inflammatory cytokines by blocking NF-kB pathway and improve LPS-induced survival in mice”, a possible new strategy for endotoxemia, bacterial toxin in the blood [6]. No study of ivermectin in people with endotoxemia appears in the research gathered here. Two more toxin studies in mice are described below, under Related Avermectins (abamectin, a relative) and P2X4 Receptors and Bacterial Killing, which also covers ivermectin in mice with sepsis.

Studies in Immune Cells

Much of the evidence on how ivermectin might act comes from immune cells grown in the laboratory. None of these results comes from a person.

Mouse macrophages: nitric oxide, prostaglandin E2 and MAPK

In a 2009 laboratory study by the same group, ivermectin inhibited the lipopolysaccharide-triggered production of nitric oxide (a gas released in large amounts during inflammation) and prostaglandin E2 (a hormone-like fat that drives swelling, fever and pain) in RAW 264.7 mouse macrophages [7]. In a concentration-dependent way it lowered the protein and gene messages of the enzymes that make them, inducible nitric oxide synthase and COX-2 (an enzyme also blocked by common anti-inflammatory painkillers). It also suppressed the switching-on (phosphorylation) of three MAPK relay proteins: p38, extracellular signal-regulated kinase (ERK1/2) and c-Jun N-terminal kinase (JNK). The authors conclude that ivermectin acts by blocking this MAPK relay [7].

Rat liver macrophages and chloride channels

Two 2003 laboratory reports studied Kupffer cells (liver macrophages); the first used cells from rats, grown in culture [8][9]. Ivermectin alone did not change the cells’ functional state [8] or their ability to engulf particles [9]. Given before lipopolysaccharide (at 1 millimolar), it significantly blocked the cells’ response: less TNF-alpha, nitric oxide and prostaglandin E2, and a smaller rise of calcium inside the cells. Removing chloride from the surrounding fluid abolished these effects completely, and the reports suggest that ivermectin acts through glycine-gated chloride channels [8][9]. A 2021 editorial on coronavirus disease 2019 (COVID-19), an opinion piece with no abstract in PubMed, carries the same idea in its title: “Anti-inflammatory activity of ivermectin in late-stage COVID-19 may reflect activation of systemic glycine receptors” [10].

Integrins in a cell-free test

Integrins are cell-surface proteins that grip surroundings and receive signals; a 2025 study reports that inflammatory cytokines, TNF-alpha among them, switch them on by binding a second site (site 2) [11]. A computer docking simulation predicted that ivermectin binds site 2, and in cell-free tests (purified proteins, no living cells) it suppressed the switching-on of beta-3 integrins by these cytokines, more at higher doses: this “may be a potential mechanism of anti-inflammatory action of ivermectin”, the authors propose [11].

Horse white blood cells: the opposite result

A 2026 laboratory study added ivermectin (2 and 4 micrograms per millilitre) to white blood cells from six healthy horses, then stimulated them with lipopolysaccharide and nigericin, another inflammation trigger [5]. Ivermectin significantly increased the gene messages for IL-1 beta, IL-6 and interleukin 8 (IL-8), without harming the cells. The authors call this “novel evidence of a pro-inflammatory transcriptional effect of ivermectin in equine leucocytes”, note that they measured gene messages only, not proteins, and call for studies at concentrations actually reached in the body [5].

The NF-kappa-B Pathway

NF-kappa-B waits in the body of the cell. When the cell meets a threat such as a bacterial toxin, it moves into the nucleus, the cell’s control centre, and turns on genes for inflammatory cytokines. A 2024 review links ivermectin’s blocking of this pathway to its anti-inflammatory role in rosacea [1], a 2025 review lists ivermectin among deworming drugs that reduce NF-kappa-B in the nucleus [4], and the 2008 study saw the block in mouse macrophages [6]. Four animal studies, each in a different organ, found lower NF-kappa-B activity together with less inflammation. All four are in mice or rats.

Heart inflammation in mice

A 2024 study used two mouse models of myocarditis (inflammation of the heart muscle): one caused by coxsackievirus B3, and one in which the immune system is provoked to attack the heart [12]. The authors describe ivermectin as an inhibitor of importin-mediated transport into the nucleus (importins are carrier proteins that ferry other proteins into it). In the mice, ivermectin improved heart function and reduced heart inflammation in both models; IL-1 beta, IL-6 and TNF-alpha fell through blocking of NF-kappa-B’s move into the nucleus of macrophages, a block also seen in virus-infected mouse macrophages in the laboratory. The authors suggest a potential application in acute myocarditis [12].

Colitis in rats

A 2022 study caused colitis (inflammation of the large bowel) with acetic acid in 78 male rats, then gave ivermectin, baclofen (a drug that activates gamma-aminobutyric acid type B, or GABA-B, receptors) or both by mouth for 5 days [13]. The ulcer index, a bowel-damage score, was 6.5 ± 0.7 in untreated (vehicle-only) rats with colitis, against 1.4 ± 0.4 with ivermectin at 0.5 mg/kg a day, 1.7 ± 0.6 with baclofen at 0.5 mg/kg a day, and 1.4 ± 0.3 with both at 0.2 mg/kg a day each. These groups also had less inflammation under the microscope and lower activated NF-kappa-B, COX-2, inducible nitric oxide synthase, TNF-alpha and myeloperoxidase (a marker of white blood cells in the tissue). The authors suggest that GABA-B receptors are involved [13].

Lung scarring in rats

A 2023 study gave rats bleomycin, a cancer medicine that scars the lungs, to model pulmonary fibrosis, and treated them with ivermectin at 0.6 mg/kg [14]. Ivermectin reduced inflammatory cells in the lungs, the inflammation and fibrosis scores, collagen, and the scarring proteins transforming growth factor beta 1 and fibronectin. It suppressed the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome, a protein complex that switches on IL-1 beta, and lowered IL-1 beta, NF-kappa-B, hypoxia-inducible factor 1 alpha, oxidative stress and markers of cell death [14].

Psoriasis-like skin in rats

A 2025 study in 15 rats caused psoriasis-like lesions with imiquimod, a medicine applied to the skin, and treated one group of 5 with 1% ivermectin gel daily from day 3 to day 7 [15]. Compared with untreated rats with lesions, the gel significantly lowered the average Psoriasis Area Severity Index score (redness, silver scale and skin thickness), lowered Toll-like receptor 4 (a danger sensor on cells) and the p65 part of NF-kappa-B, and reduced skin thickening, scarring in the deeper skin and inflammatory cells [15].

Allergic Inflammation in the Airways and Skin

In an allergy, the immune system reacts against a harmless substance. Two mouse studies tested ivermectin in allergic inflammation; neither has been repeated in people in the research gathered here.

Allergic asthma in mice

A 2011 study made mice allergic to ovalbumin, an egg-white protein, then challenged them with it, causing allergic airway inflammation and airway remodelling (lasting structural change) [16]. Given 1 hour before the challenge at 2 mg/kg, ivermectin significantly reduced the immune cells drawn into the airways, the cytokines in fluid washed from the lungs and the blood levels of two antibodies against ovalbumin (immunoglobulin E and immunoglobulin G1), and suppressed excess mucus from the goblet cells of the airway lining. The authors suggest ivermectin may be effective in non-infectious airway inflammatory diseases “such as allergic asthma” [16]. A 2025 review likewise lists ivermectin among drugs that reduced mucus, cytokines and airway narrowing in experimental lung inflammation [4].

Allergic skin inflammation in mice

A 2017 study produced atopic dermatitis (eczema) in mice by repeated exposure to the house dust mite Dermatophagoides farinae [17]. Ivermectin applied to the skin improved the inflammation by reducing the priming and activation of T cells (white blood cells that direct the immune attack) aimed at the allergen, and the production of inflammatory cytokines. It had no major effect on dendritic cells, which show allergens to T cells, but impaired T-cell activation, multiplication and cytokine production. The authors conclude that ivermectin “is endowed with topical anti-inflammatory properties that could have important applications for the treatment of T-cell-mediated skin inflammatory diseases” [17].

Rosacea: Anti-Inflammatory Action in Human Skin

Rosacea is a long-lasting skin disorder, mainly of the face, with passing or persistent redness, small visible blood vessels, swelling and inflamed spots (papules and pustules) [18]. It affects up to 10% of the world population, especially fair-skinned people aged 35 to 50 and women more often than men, and topical ivermectin is among its newer treatments [18]. In the research gathered here, it is the main inflammatory disease in which ivermectin has been tested in controlled trials in people.

Two actions in one cream

There is accumulating evidence that the Demodex mite, which normally lives in human skin, is linked to papulopustular rosacea, the form with inflamed spots [19]. The mites live in the hair follicles and their oil glands, and ivermectin kills them [3]. The reviews credit the cream with two actions. A 2018 systematic review says it has “both anti-inflammatory and acaricidal activity against Demodex mites” (acaricidal: mite-killing), and that the established treatments, metronidazole, azelaic acid and tetracyclines, are thought to work through anti-inflammatory effects [19]. A 2015 review says both actions “may contribute” to its efficacy [20]. Another 2015 review names changes in the innate (first-line) immune system among the processes that may be involved, with the mites possibly playing a role in them [21], and a 2015 article states that “inflammatory mechanisms appear to play a dominant role in the development of rosacea inflammatory lesions” [3].

What the trials in people found

Separating mite-killing from calming inflammation

The mite-killing action has been measured in people. A 2025 meta-analysis of five studies with 180 participants found that daily ivermectin 1% cream significantly reduced Demodex counts or density in every study, on average by 70.01 mites per square centimetre, with an 80% decrease in mite-positive results (5 or more per square centimetre) [22]. The effects of a 16-week course lasted up to 12 weeks after treatment, side effects were mild and local, mites can repopulate, and the authors call for cautious interpretation of the few, varied studies. The mites can also contribute to blepharitis (inflamed eyelid margins) [22].

The anti-inflammatory action has not been measured directly in people: the trials counted spots and rated severity, and none of the human studies gathered here measured cytokines or NF-kappa-B in rosacea skin. Fewer spots could come from fewer mites, calmer inflammation, or both. The 2018 review concludes that more research is needed on the clinical benefit of the mite-killing action in preventing relapse [19]. The NF-kappa-B explanation [1] agrees with the animal and cell findings above, but no rosacea trial gathered here tested it in human skin.

P2X4 Receptors and Bacterial Killing

Here ivermectin works the other way: it strengthens a receptor instead of blocking a pathway. P2X4 receptors are channels on macrophages that open when they detect adenosine triphosphate (ATP), the cell’s energy molecule, which damaged cells release as an alarm signal.

The 2018 sepsis study in mice

Impaired macrophage function is a primary cause of immune paralysis, organ injury and death in sepsis, a life-threatening reaction to infection [23]. In this 2018 study, ATP helped macrophages kill sepsis-causing bacteria through P2X4 receptors in a laboratory killing test; ATP outside cells rose during sepsis in mice; and mice lacking P2X4 receptors confirmed the receptors’ role in killing bacteria and protecting against organ injury and death. Macrophages were essential for the antibacterial, anti-inflammatory and organ-protective effects of P2X4 in sepsis. Ivermectin, an allosteric activator of P2X4 (it binds the receptor at a second spot and makes it respond more strongly to ATP), “protects against bacterial dissemination and mortality in sepsis”: in the mice, it protected against the spread of bacteria and against death [23]. The authors propose P2X4 as a drug target in sepsis and other infections; no study of ivermectin in people with sepsis appears in the research gathered here. Ivermectin: Antibacterial Research covers ivermectin and bacteria.

Human cells compared with mouse and rat cells

In human macrophages grown in the laboratory, ivermectin (3 micromolar) strengthened an electrical current resembling the P2X4 receptor’s [24]. A 2012 laboratory study found that it also strengthened currents through a related receptor, P2X7, in human macrophages, while on rat or mouse P2X7 it was only poorly effective, a species-specific action [25].

When strengthening P2X4 feeds inflammation

A 2021 laboratory study describes P2X4 as “involved in neuropathic pain, inflammation and arterial tone”. In human macrophages it drove the release of a chemokine (a signal that draws white blood cells into tissue), and a natural compound, taspine, blocked this “pro-inflammatory signalling by P2X4” and reversed ivermectin’s strengthening of P2X4 currents in engineered cells [26]. In a 2026 study in mice, daily lipopolysaccharide injections caused depression-like behaviour and brain inflammation, which low-intensity pulsed ultrasound over the hippocampus (a memory and mood region of the brain) reduced; ivermectin, given as a P2X4 activator, significantly weakened the ultrasound’s anti-inflammatory, nerve-protecting and antidepressant effects [27]. In the mouse brain, ivermectin worked against an anti-inflammatory treatment.

Related Avermectins

Ivermectin is a derivative of the avermectin family [1][20]. Two relatives have been studied for inflammation, with results that run in opposite directions.

Avermectin in mouse macrophages

In a 2009 laboratory study, avermectin (0.625, 1.25 or 5 mg/L) given to RAW 264.7 mouse macrophages 1 hour before lipopolysaccharide significantly altered (“regulated”, the authors’ word) TNF-alpha, IL-1 beta and the anti-inflammatory cytokine interleukin 10, with no significant effect on IL-6 [28]. It inhibited NF-kappa-B’s move into the nucleus and the switching-on of JNK and p38, and the authors conclude that it may act by blocking NF-kappa-B and the MAPK relay [28].

Abamectin in lung inflammation in mice

In a 2011 study, mice given abamectin by mouth and then lipopolysaccharide (0.5 mg/kg) to cause acute lung injury were significantly protected at 2 mg/kg [29]. Fluid in the lung tissue (wet-to-dry weight ratio) fell, as did total cells, neutrophils (the most common white blood cells) and macrophages in fluid washed from the lungs. Abamectin blunted the toxin’s switching-on of p38 MAPK, ERK and inhibitor of kappa B (the protein that holds NF-kappa-B in check), and the authors conclude that it acts through the MAPK and NF-kappa-B pathways [29].

Avermectin as an insecticide in carp

Avermectin is also a widely used insecticide, and in fish it caused inflammation. In a 2022 study, carp in a 96-hour exposure test were kept in 3.005 or 12.02 micrograms per litre, below the 24.04 micrograms per litre that killed half the carp in 96 hours [30]. Avermectin built up in the brain and caused inflammatory cell infiltration, nerve-cell death, breakdown of the blood-brain barrier and oxidative stress; it brought on brain inflammation by activating NF-kappa-B and releasing IL-1 beta, IL-6, TNF-alpha and inducible nitric oxide synthase [30]. In carp brains, avermectin activated NF-kappa-B, the opposite of its effect in mouse macrophages.

What Has Been Tested in People

In the research gathered for this page, the only tests in people are of ivermectin 1% cream on the skin: trials in moderate to severe papulopustular rosacea, with extension studies of up to 52 weeks [20][19][21], and a meta-analysis of Demodex mite counts [22]. They measured spots, severity, quality of life, relapse and mites, not inflammatory signals. No trial gave ivermectin by mouth or by injection to people for an inflammatory disease. Everything else comes from mice (toxin survival, myocarditis, asthma, eczema, sepsis), rats (colitis, lung scarring, psoriasis-like skin), animal and human cells in the laboratory, a cell-free test, fish, and one opinion editorial.

The studies themselves point to three reasons why animal and cell findings may not carry over to people:

Inflammation of the Gums

Gum disease is an inflammatory disease: gingivitis is inflammation of the gums, and periodontitis a deeper inflammation that destroys the bone holding the teeth. None of the research gathered for this page tested ivermectin on gum inflammation, in people, in animals or in gum cells in the laboratory; the findings above come from other organs of animals, from cells in the laboratory, and from the facial skin of people with rosacea. The page Ivermectin for Gum Disease gathers what people report about ivermectin and their gums, and the published case reports of ivermectin against parasites in gum tissue.

Key Research Papers

  1. Kaur B, Blavo C, Parmar MS. Ivermectin: A Multifaceted Drug With a Potential Beyond Anti-parasitic Therapy. Cureus. 2024;16(3):e56025. PubMed PMID: 38606261
  2. Zargari O, Aghazadeh N, Moeineddin F. Clinical applications of topical ivermectin in dermatology. Dermatol Online J. 2016;22(9). PubMed PMID: 28329606
  3. Abokwidir M, Fleischer AB. An emerging treatment: Topical ivermectin for papulopustular rosacea. J Dermatolog Treat. 2015;26(4):379-80. PubMed PMID: 25424053
  4. Rodrigues DCDN, Porto JCS, Dos Santos IL, Filho JIAB, Ferreira PMP. Repositioning anthelmintics for the treatment of inflammatory-based pathological conditions. Inflammopharmacology. 2025;33(2):551-571. PubMed PMID: 39589670
  5. Apaoblaza S, Albornoz A, Henriquez C, Quiroga J, Burgos RA, Moran G. Ivermectin enhances the transcription of pro-inflammatory cytokines in equine leukocytes stimulated with LPS and nigericin. Vet Anim Sci. 2026;34:100894. PubMed PMID: 42927118
  6. Zhang X, Song Y, Ci X, An N, Ju Y, Li H, et al. Ivermectin inhibits LPS-induced production of inflammatory cytokines and improves LPS-induced survival in mice. Inflamm Res. 2008;57(11):524-9. PubMed PMID: 19109745
  7. Zhang X, Song Y, Xiong H, Ci X, Li H, Yu L, et al. Inhibitory effects of ivermectin on nitric oxide and prostaglandin E2 production in LPS-stimulated RAW 264.7 macrophages. Int Immunopharmacol. 2009;9(3):354-9. PubMed PMID: 19168156
  8. Viktorov AV. [Ivermectin inhibits activation of Kupffer cells induced by lipopolysaccharide toxin]. Antibiot Khimioter. 2003;48(4):3-6. PubMed PMID: 13677129
  9. Viktorov AV, Yurkiv VA. Effect of ivermectin on function of liver macrophages. Bull Exp Biol Med. 2003;136(6):569-71. PubMed PMID: 15500074
  10. DiNicolantonio JJ, Barroso-Aranda J, McCarty MF. Anti-inflammatory activity of ivermectin in late-stage COVID-19 may reflect activation of systemic glycine receptors. Open Heart. 2021;8(1). PubMed PMID: 33875563
  11. Takada YK, Takada Y. Ivermectin Binds to the Allosteric Site (Site 2) and Inhibits Allosteric Integrin Activation by TNF and Other Pro-Inflammatory Cytokines. Int J Mol Sci. 2025;26(17). PubMed PMID: 40943574
  12. Gao X, Xuan Y, Zhou Z, Chen C, Wen Wang D, Wen Z. Ivermectin ameliorates acute myocarditis via the inhibition of importin-mediated nuclear translocation of NF-κB/p65. Int Immunopharmacol. 2024;133:112073. PubMed PMID: 38636372
  13. Aryannejad A, Tabary M, Noroozi N, Mashinchi B, Iranshahi S, Tavangar SM, et al. Anti-inflammatory Effects of Ivermectin in the Treatment of Acetic Acid-Induced Colitis in Rats: Involvement of GABAB Receptors. Dig Dis Sci. 2022;67(8):3672-3682. PubMed PMID: 34674071
  14. Abd-Elmawla MA, Ghaiad HR, Gad ES, Ahmed KA, Abdelmonem M. Suppression of NLRP3 inflammasome by ivermectin ameliorates bleomycin-induced pulmonary fibrosis. J Zhejiang Univ Sci B. 2023;24(8):723-733. PubMed PMID: 37551558
  15. Noori T, Sureda A, Shirooie S. Ivermectin decreases inflammation and imiquimod-induced psoriasis-like skin lesions in rat via targeting TLR4/p65 NF-κB. Iran J Basic Med Sci. 2025;28(6):808-814. PubMed PMID: 40343294
  16. Yan S, Ci X, Chen N, Chen C, Li X, Chu X, et al. Anti-inflammatory effects of ivermectin in mouse model of allergic asthma. Inflamm Res. 2011;60(6):589-96. PubMed PMID: 21279416
  17. Ventre E, Rozières A, Lenief V, Albert F, Rossio P, Laoubi L, et al. Topical ivermectin improves allergic skin inflammation. Allergy. 2017;72(8):1212-1221. PubMed PMID: 28052336
  18. Sharma A, Kroumpouzos G, Kassir M, Galadari H, Goren A, Grabbe S, et al. Rosacea management: A comprehensive review. J Cosmet Dermatol. 2022;21(5):1895-1904. PubMed PMID: 35104917
  19. Ebbelaar CCF, Venema AW, Van Dijk MR. Topical Ivermectin in the Treatment of Papulopustular Rosacea: A Systematic Review of Evidence and Clinical Guideline Recommendations. Dermatol Ther (Heidelb). 2018;8(3):379-387. PubMed PMID: 29943217
  20. Deeks ED. Ivermectin: A Review in Rosacea. Am J Clin Dermatol. 2015;16(5):447-52. PubMed PMID: 26254001
  21. Ali ST, Alinia H, Feldman SR. The treatment of rosacea with topical ivermectin. Drugs Today (Barc). 2015;51(4):243-50. PubMed PMID: 26020066
  22. Paichitrojjana A, Khuancharee K, Paichitrojjana A. Efficacy of topical Ivermectin in controlling human Demodex infestation: Evidence from systematic review and meta-analysis. Parasite Epidemiol Control. 2025;31:e00461. PubMed PMID: 41103378
  23. Csóka B, Németh ZH, Szabó I, Davies DL, Varga ZV, Pálóczi J, et al. Macrophage P2X4 receptors augment bacterial killing and protect against sepsis. JCI Insight. 2018;3(11). PubMed PMID: 29875325
  24. Vargas-Martínez EM, Gómez-Coronado KS, Espinosa-Luna R, Valdez-Morales EE, Barrios-García T, Barajas-Espinosa A, et al. Functional expression of P2X1, P2X4 and P2X7 purinergic receptors in human monocyte-derived macrophages. Eur J Pharmacol. 2020;888:173460. PubMed PMID: 32805257
  25. Nörenberg W, Sobottka H, Hempel C, Plötz T, Fischer W, Schmalzing G, et al. Positive allosteric modulation by ivermectin of human but not murine P2X7 receptors. Br J Pharmacol. 2012;167(1):48-66. PubMed PMID: 22506590
  26. Nadzirin IB, Fortuny-Gomez A, Ngum N, Richards D, Ali S, Searcey M, et al. Taspine is a natural product that suppresses P2X4 receptor activity via phosphoinositide 3-kinase inhibition. Br J Pharmacol. 2021;178(24):4859-4872. PubMed PMID: 34398973
  27. Wang Y, Meng X, Zhang X, Chen R, Zhang M, Yang D, et al. Low-Intensity Pulsed Ultrasound Alleviation of LPS-Induced Depression-Like Behavior via Microglial P2X4R Inhibition and BDNF/TrkB Pathway Activation. CNS Neurosci Ther. 2026;32(2):e70786. PubMed PMID: 41674056
  28. Ci X, Li H, Yu Q, Zhang X, Yu L, Chen N, et al. Avermectin exerts anti-inflammatory effect by downregulating the nuclear transcription factor kappa-B and mitogen-activated protein kinase activation pathway. Fundam Clin Pharmacol. 2009;23(4):449-55. PubMed PMID: 19453757
  29. Zhang X, Li J, Chen C, Ci X, Yu Q, Zhang X, et al. Protective effect of abamectin on acute lung injury induced by lipopolysaccharide in mice. Fundam Clin Pharmacol. 2011;25(6):700-7. PubMed PMID: 21118302
  30. Zhang T, Dong Z, Liu F, Pan E, He N, Ma F, et al. Avermectin induces carp neurotoxicity by mediating blood-brain barrier dysfunction, oxidative stress, inflammation, and apoptosis through PI3K/Akt and NF-κB pathways. Ecotoxicol Environ Saf. 2022;243:113961. PubMed PMID: 35969982

PubMed Topic Searches

  1. PubMed: Ivermectin anti-inflammatory
  2. PubMed: Ivermectin and NF-kappa-B
  3. PubMed: Ivermectin and lipopolysaccharide
  4. PubMed: Topical ivermectin and rosacea
  5. PubMed: Ivermectin and P2X4 receptors
  6. PubMed: Avermectin and inflammation

Back to Table of Contents

Connections

Back to Table of Contents