Table 2 Summary of natural products/molecules targeting C. acnes in acne treatment

Toona sinensis extract

C. acnes-treated HaCaT cells

Its extract shows antibacterial and anti-inflammatory effects on C. acnes-induced keratinocytes

[108]

Nicotinamide

HaCaT cells and primary keratinocytes stimulated by C. acnes

Nicotinamide decreases inflammatory IL-8 production in C. acnes-stimulated keratinocytes

[109]

Piceatannol (PCT) and Orobol

C. acnes-induced HaCaT keratinocytes

PCT and orobol alleviate the inflammation and hyperkeratinization mediated by C. acnes in keratinocytes

[110, 111]

Licochalcone A

C. acnes-treated primary mouse macrophages and human SZ95 sebocytes, and C. acnes-induced skin inflammation in mice

It blocks C. acnes-induced inflammation in macrophages and sebocytes. Moreover, its topically application attenuates C. acnes-induced skin inflammation in mice

[112]

Schisandrin A, B, and C

C. acnes-infected THP-1 cells

Schisandrin A, B, and C inhibit C. acnes-induced pyroptosis and inflammation via NLRP3 pathway

[113]

Baicalin and Polyphyllin I

C. acnes-induced THP-1 cells and HaCaT cells, and C. acnes-injected rats used as the acne model

Baicalin and Polyphyllin I alleviate C. acnes-induced inflammation through modulating the NLRP3 pathway

[114,115,116]

SIG1273 and SIG1459

Human keratinocytes exposed to C. acnes, a randomized and double-blind controlled trial, and a vehicle controlled head-to-head comparison between SIG1459 and 3% BPO

Both SIG1273 and SIG1459 combat against C. acnes. Meanwhile, both of them improve the clinical outcome of acne, with well tolerance. Moreover, 1% SIG1459 outperforms 3% BPO in a head-to-head comparison against BPO

[117, 118]

Myricetin

C. acnes-stimulated human SZ95 sebocytes

Myricetin inhibits the C. acnes-stimulated inflammation in sebocytes via suppressing the TLR2 and rapamycin pathways

[119]

Quercetin

C. acnes-stimulated HaCaT, THP-1 and RAW 264.7 cells, and C. acnes-induced skin inflammation in mice

Quercetin suppresses the C. acnes-mediated inflammation via inhibiting the TLR-2 and MAPK pathways in vitro. In vivo, quercetin reduces mouse cutaneous erythema and swelling induced by C. acnes

[120]

The extract of Helichrysum odoratissimum (L.) Sweet

C. acnes-induced HaCaT cells

It prevents the biofilm formation of C. acnes, controls C. acnes proliferation, and exhibits inhibitory activity on factors associated with bacterial virulence

[121]

Arctostaphylos uva-ursi leaf extract

HaCaT cells and HaCaT cells cotreatment with heat-killed C. acnes

It decreases the C. acnes-induced inflammation. Moreover, it disrupts the biofilm formation of C. acnes without affecting keratinocyte growth

[122]

3,3'-diindolylmethane (DIM)

Planktonic cells/NA

DIM inhibits biofilm formation by C. acnes without affecting the viability of cell growth. Also, DIM inhibits the biofilm formation of multiple other species. Moreover, DIM inhibits the expression of biofilm-related genes in C. acnes

[123]

G2 dendrigraft of lysine dendrimer (G2)

Human skin explants

G2 modifies the biofilm formation of C. acnes. Additionally, G2 decreases the inflammation and improves skin desquamation after C. acnes colonization. Moreover, G2 increases the diversity of C. acnes, with a modification of the balance between C. acnes phylotypes

[124]

Kaempferia parviflora

C. acnes-stimulated HaCaT cells and IGF-1 induced sebocytes

Kaempferia parviflora modulates the inflammatory signals in C. acnes-stimulated HaCaT cells and inhibits the lipogenesis of sebocytes

[125]

Mangifera indica leave

Sebocytes and sebaceous glands from skin explants

It reduces the C. acnes lipase activity from a severe acne phylotype. Additionally, it protects the microbiota equilibrium

[126]

Bee venom (BV) and melittin

Models of IGF-1 or C. acnes-induced lipogenic skin disease

In the C. acnes-induced mouse model, BV and melittin decrease the transcriptions of genes involved in lipid biosynthesis and inflammation mediated by C. acnes

[127, 128]