Skin (Integumentary System)

Wound healing runs through inflammation, proliferation and remodelling, and the vulnerary herbs act mostly on the second phase.

Gotu kola is the best-characterised of them. Its triterpenes asiaticoside and madecassoside stimulate fibroblast proliferation and type I collagen synthesis, and madecassoside accelerates burn wound healing in mice ^{19Reference 19Liu et al. · 2008AnimalMadecassoside isolated from Centella asiatica facilitates burn wound healing in mice — animal modelView study →}.

Dragon’s blood sap carries taspine, isolated in 1989 as the sap’s cicatrizant principle, which promotes fibroblast migration into the wound bed in animal models ^{67Reference 67Vaisberg et al. · 1989AnimalTaspine is the cicatrizant principle in sangre de grado extracted from Croton lechleri — animal model in vivoView study →} and is separately anti-inflammatory ^{68Reference 68Perdue et al. · 1979AnimalSouth American plants II: taspine isolation and anti-inflammatory activity — animal model in vivoView study →}. Calendula tincture drives fibroblast proliferation through PI3K signalling, and comfrey extract induces measurable epidermal regeneration in human skin models ^{15Reference 15Dähnhardt et al. · 2020In vitroEpidermal regeneration induced by comfrey extract — in vitro light and electron microscopyView study →}.

Two herbs work the other end of the same phase. Lady’s mantle’s quercetin-3-O-β-glucuronide inhibits collagenase, the enzyme that degrades newly laid collagen, out-performing doxycycline in vitro ^{69Reference 69Mandrone et al. · 2018In vitroIdentification of a collagenase-inhibiting flavonoid from Alchemilla vulgaris using NMR-based metabolomics — in vitroView study →}, which makes it a matrix-preserving herb rather than a matrix-building one.

Fireweed’s hyperoside does the same job against hyaluronidase and collagenase together ^{70Reference 70Gevrenova et al. · 2025In vitroPhytochemical profile and biological insights of Epilobium angustifolium L. herb — antioxidant and enzyme-inhibition assays, in vitroView study →}.

Anything that drives fibroblast activity has a theoretical capacity to worsen hypertrophic scarring.

The most physical mechanism in the skin materia medica, and it has four arms at once.

Honey’s high sugar concentration draws water osmotically out of bacterial cells, and its pH of around 3.5 to 4.5 is hostile to most wound pathogens. Glucose oxidase in the honey generates low, sustained hydrogen peroxide.

Manuka adds a fourth component that is not peroxide-dependent, methylglyoxal, derived from dihydroxyacetone in Leptospermum nectar, which is what the UMF rating measures.

That combination is why honey retains activity against antibiotic-resistant organisms.

It is also why the medical-grade product is gamma-irradiated, since raw honey can carry Clostridium botulinum spores.

Tannins are polyphenols that bind and precipitate surface proteins, forming a thin protective layer over damaged tissue that reduces exudate, seals capillaries and creates a physical barrier.

Witch hazel’s highly galloylated tannins also have direct antioxidant activity in skin cells and impair the keratinocyte inflammatory cascade typical of atopic eczema ^{28Reference 28Piazza et al. · 2022In vitroWitch hazel (Hamamelis virginiana L.) bark extract impairs the keratinocyte inflammatory cascade typical of atopic eczema — in vitroView study →}. The tannins live in the bark and leaf, and the steam distillate sold as “witch hazel water” contains almost none, so the astringency explanation may not be the whole account of what the trials measured.

Where the tannin load is high enough the layer stops being a film and becomes a structure. Barbatimão bark, one of the most condensed-tannin-dense materials in use anywhere, precipitates enough surface protein to form a coagulum that acts as barrier, haemostat and scaffold at once.

The route argument matters more here than anywhere else in herbal medicine. Tannins are large, poorly absorbed polyphenols, which is a fatal limitation when they are swallowed and a non-issue when they are not, since nothing needs to be absorbed for an astringent to work on the tissue it is touching.

The European regulator recognises oak bark for topical use in weeping skin inflammation on exactly that reasoning ^{71Reference 71European Medicines Agency · 2009ReviewCommunity herbal monograph on Quercus robur L., QView study →}, while capping the same herb’s internal use at a few days.

The mechanism that puts these herbs into competition with hydrocortisone.

Calendula’s triterpenoid faradiol esters are its principal topical anti-inflammatory constituents, demonstrated by fractionation ^{12Reference 12Della Loggia et al. · 1994In vitroThe role of triterpenoids in the topical anti-inflammatory activity of Calendula officinalis flowers — in vitro and animal modelView study →}. Chamomile contributes bisabolol and chamazulene, and comfrey root extract inhibits NF-κB signalling at two distinct steps.

Oregon grape supplies the most specific version of this: its bisbenzylisoquinoline alkaloids berbamine and oxyacanthine inhibit 5-lipoxygenase ^{72,73Reference 72Müller et al. · 1994In vitroThe antipsoriatic Mahonia aquifolium and its active constituents I — pro- and antioxidant properties and inhibition of 5-lipoxygenase, in vitroView study →Reference 73Bezáková et al. · 1996In vitroLipoxygenase inhibition and antioxidant properties of bisbenzylisoquinoline alkaloids isolated from Mahonia aquifolium — in vitroView study →} while a separate fraction suppresses keratinocyte proliferation ^{74Reference 74Müller et al. · 1995In vitroThe antipsoriatic Mahonia aquifolium and its active constituents II — antiproliferative activity against human keratinocytes, in vitroView study →}, two mechanisms aimed at the two halves of what a psoriatic plaque is doing. Douglas fir needle oil is the same idea tested in the right cell type, showing anti-inflammatory and anti-proliferative activity in cultured human dermal fibroblasts ^{75Reference 75Han et al. · 2017In vitroIn vitro biological activities of Douglas fir essential oil in a human skin disease model — in vitro, human dermal fibroblastsView study →}.

What distinguishes these from corticosteroids is what they lack. No skin thinning, no telangiectasia, no adrenal suppression and no rebound on withdrawal, which is why a herb that only matches a mild steroid over four weeks may still be preferable over four months.

The one skin mechanism that works from the inside.

Polypodium leucotomos extract taken orally reduces the erythema, DNA damage and Langerhans-cell depletion caused by ultraviolet exposure ^{53Reference 53González et al. · 1997RCTTopical or oral administration with an extract of Polypodium leucotomos prevents acute sunburn and psoralen-induced phototoxic reactions — randomised trialView study →}. The route combines free-radical scavenging, inhibition of UV-induced matrix metalloproteinases, and preservation of cutaneous immune surveillance, since ultraviolet exposure is locally immunosuppressive.

That third arm is why the same extract has been trialled in photodermatoses, melasma and as an adjunct to phototherapy in vitiligo.

It is not a sunscreen and does not replace one.

The skin-infection mechanism, and almost all of it is laboratory work.

Horopito’s polygodial is a sesquiterpene dialdehyde that disrupts fungal plasma membrane function, with in vitro activity against Candida albicans established since the early 1980s ^{46,47,48Reference 46McCallion et al. · 1982In vitroAntibiotic substances from New Zealand plantsView study →Reference 47Lee et al. · 1999In vitroIn vitro antifungal susceptibilities of Candida albicans and other fungal pathogens to polygodial, a sesquiterpene dialdehyde — in vitroView study →Reference 48Kubo et al. · 2001In vitroAntifungal mechanism of polygodial — in vitroView study →}. Usnic acid disrupts bacterial membranes and inhibits biofilm formation, including in methicillin-resistant Staphylococcus aureus ^{49,50Reference 49Pompilio et al. · 2016In vitroAntibacterial and antibiofilm mechanisms of usnic acid against methicillin-resistant Staphylococcus aureus — in vitroView study →Reference 50Francolini et al. · 2004In vitroUsnic acid, a natural antimicrobial agent able to inhibit bacterial biofilm formation on polymer surfaces — in vitroView study →}.

Biofilm activity matters disproportionately in skin and wound infection, where established biofilm is a principal reason chronic wounds fail to close.

A subset of these compounds only works in the light, which sounds like a disqualifier and on this one organ is not. Prickly ash’s furanocoumarins inhibit a broad fungal panel in vitro ^{76Reference 76Bafi-Yeboa et al. · 2005In vitroAntifungal constituents of northern prickly ash, Zanthoxylum americanum Mill. — in vitroView study →}, and the thiophenes of balsamroot root, a family of Asteraceae compounds whose antimicrobial potency rises sharply under ultraviolet, sit behind that plant’s antifungal and antibacterial screening results ^{77,78Reference 77Matsuura et al. · 1996In vitroAn antibacterial thiophene from Balsamorhiza sagittata — in vitro isolation studyView study →Reference 78McCutcheon et al. · 1994In vitroAntifungal screening of medicinal plants of British Columbian native peoples — in vitro screenView study →}.

Skin is the one tissue a photoactivated antimicrobial can reach in daylight.

The same chemistry is why both plants cause phytophotodermatitis. Furanocoumarins on skin plus sunlight is the classic recipe for a delayed burn, so the therapeutic effect and the injury are the same event under different conditions.

None of this establishes a clinical antifungal.

The one mechanism aimed at a skin structure rather than at the skin surface, and it separates a traditional category into two unrelated things wearing one name.

Eccrine sweat glands are cholinergically innervated, an oddity of the autonomic nervous system, since they are sympathetic fibres releasing acetylcholine. A muscarinic agonist therefore drives them directly.

Pilocarpine, the alkaloid of jaborandi leaf, does exactly that, and does it reliably enough that pilocarpine iontophoresis is still the standard way to raise sweat for cystic-fibrosis chloride testing ^{79,80Reference 79LeVeque et al. · 1993RCTA multicenter, randomized, double-blind, placebo-controlled, dose-titration study of oral pilocarpine — randomised controlled trial establishing muscarinic gland stimulation and its cholinergic sweating effectView study →Reference 80Rieke et al. · 1995RCTOral pilocarpine for radiation-induced xerostomia — integrated efficacy and safety results from two prospective randomised clinical trialsView study →}.

Every other diaphoretic works some other way. Yarrow, elder and ginger open the peripheral circulation and let the body sweat as a consequence, so the effect depends on being warm, on being hydrated and on the thermoregulatory response cooperating.

The two categories fail differently. A circulatory diaphoretic does nothing to a cold, shut-down patient, while a muscarinic agonist floods a person whose gland tissue is intact, and profuse sweating is simultaneously the intended effect and the first sign of cholinergic overdose.

The traditional explanation is wrong, and something may still be happening.

There is no metabolic backlog for a herb to flush. But chronic inflammatory skin disease is systemic, since psoriasis is an IL-17-driven immune condition with cardiovascular comorbidity and atopic eczema involves systemic Th2 activation, and several classic alteratives have measurable immune effects.

Smilax species suppress IL-17-driven T-cell responses in psoriasis models ^{42Reference 42Guo et al. · 2024AnimalIntegrated network pharmacological analysis revealed that Smilax glabra Roxb. alleviates IMQ-induced psoriatic skin inflammation through regulating T cell immune response — animal modelView study →}. Burdock has anti-acne activity in vitro attributed to root peptides ^{61Reference 61Miazga-Karska et al. · 2020In vitroAnti-acne action of peptides isolated from burdock root — in vitro and pilot testingView study →}, and its lignan arctiin protects dermal fibroblasts against UVB ^{62Reference 62Lee et al. · 2014In vitroArctiin induces a UVB protective effect in human dermal fibroblast cells through microRNA expression — in vitroView study →}.

That is a much more modest and more plausible claim than blood cleansing, and it is still preclinical.