Multifunctional Dermatological Effects of Whole-Plant Bassia scoparia Extract: Skin Repair and Protection

Abstract

Bassia scoparia (Syn. Kochia scoparia (L.) Schrad.) is a medicinal plant whose fruit, Kochiae Fructus, has been extensively studied for its dermatological applications. This study focused on extracts from the whole plant B. scoparia (WPBS), excluding fruits, to address the research gap regarding the medicinal properties of non-fruit parts. The diverse skin benefits of WPBS, including its anti-photoaging, moisturizing, wound healing, anti-inflammatory, and anti-angiogenic effects, were investigated. The WPBS extract enhanced the viability of keratinocytes (HaCaT) without inducing cytotoxic effects. WPBS significantly reduced matrix metalloproteinase-1 (MMP-1) levels and increased collagen type I alpha 1 (COL1A1) levels (p < 0.01) in fibroblasts exposed to ultraviolet B (UVB) radiation, indicating strong anti-photoaging effects. WPBS upregulated skin hydration markers such as aquaporin-3 (AQP3) and hyaluronan synthase-3 (HAS3) and effectively accelerated fibroblast wound closure compared to the positive control. Furthermore, WPBS substantially downregulated the expression of inflammatory (COX-2 and IL-1β) and angiogenic markers (VEGF). Transcriptome analysis (RNA-seq) confirmed that WPBS suppressed inflammation-related and UV-induced gene expression pathways. Overall, these findings expand the therapeutic scope of B. scoparia beyond its traditional fruit use and suggest that WPBS is a promising botanical ingredient for various skin applications.

Keywords: anti-angiogenic; anti-inflammatory; anti-photoaging; skin hydration; whole-plant Bassia scoparia; wound healing.

Figure 1

Experimental workflow and study design for WPBS biological evaluation. WPBS extract was prepared via ultrasonic aqueous extraction of Bassia scoparia excluding fruits, followed by LC-QTOF-MS component analysis. Biological evaluation was conducted using keratinocyte and fibroblast cell lines to assess dermatological effects via real-time PCR. RNA-seq analysis with DEG identification and pathway analysis was performed using DESeq2 and fgsea packages. WPBS, whole plant B. scoparia; DEGs, differentially expressed genes.

Figure 2

Bioactive compounds in whole-plant B. scoparia (WPBS) extract. The X-axis represents retention time (minutes) and the Y-axis represents peak area as relative abundance. (A) Negative ion mode analysis identified major compounds including D-xylulose, alpha-D-mannoheptulopyrranose, D-glyceric acid, ribonic acid, and gamma-aminobutyric acid (GABA). (B) Positive ion mode analysis revealed a high abundance of stigmatellin Y and 4-aminobenzoic acid (PABA), along with C16 sphinganine, adenine, butyl dodecanoate, pheophorbide a, and (E)-3-(2-hydroxyphenyl)-2-propenal. Compounds with known anti-photoaging, moisturizing, wound-healing, anti-inflammatory, and anti-angiogenic properties are highlighted in red text, and their chemical structures are shown on the right.

Figure 3

Protective effects of whole-plant B. scoparia (WPBS) extract against UVB-induced photoaging and skin hydration markers in cell culture. (A) Hs68 fibroblasts exposed to UVB irradiation (15 mJ/cm²) and MMP-1 mRNA expression compared to the non-irradiated control (None). A significant reduction in UVB-induced MMP-1 expression by WPBS treatment (10%) to a level comparable or slightly superior to that of the positive control, retinoic acid (RA, 1 μM). (B) UVB exposure induced a decrease in Collagen Type I Alpha 1 chain (COL1A1) mRNA in fibroblasts and significantly restored COL1A1 expression by WPBS (1% and 10%), with efficacy similar to RA. (C) Significantly upregulated aquaporin-3 (AQP3) mRNA in HaCaT keratinocytes treated with WPBS (1%) to a level comparable with RA (p < 0.01); no effect of 10% WPBS. (D) WPBS (1% and 10%) increased HAS3 mRNA expression with a greater effect at 1%. Statistical significance: # p < 0.05, ## p < 0.01, ### p < 0.001 vs. none; ** p < 0.01, *** p < 0.001 vs. UVB.

Figure 4

Wound-healing efficacy of WPBS in Hs68 fibroblasts. (A) Scratch-wound assay images (0 and 24 h post-wounding) showing substantially greater wound closure in fibroblasts treated with WPBS (1% or 10%) compared with that in untreated controls and comparable to that in cells treated with 10% FBS (positive control). (B) Time-course analysis of wound closure over 24 h showing that WPBS (1% and 10%) accelerated wound healing rates, closely approaching healing in the 10% FBS-treated positive control. (C) Quantification of wound closure 24 h post-scratch showing that WPBS significantly enhanced wound regeneration compared to untreated cells (~80% closure vs. ~50% in controls). Healing in the 1% WPBS-treated group was slightly better than in the 10% WPBS-treated group. Statistical significance: ** p < 0.01, *** p < 0.001, vs. none.

Figure 5

Anti-inflammatory and anti-angiogenic effects of WPBS. (A) Poly (I:C) + IL-4 induced inflammation increased COX-2 mRNA levels in HaCaT keratinocytes. WPBS (1%) treatment significantly decreased COX-2 expression compared with the stimulated control, but not as strongly as dexamethasone (1 μM, positive control). (B) Increased IL-1β mRNA in HaCaT cells following inflammation induced by poly (I:C) + IL-4 significantly reduced IL-1β expression induced by WPBS (1%). (C) Elevated VEGF mRNA levels in Hs68 fibroblasts following PGE2 stimulation (30 nM). VEGF expression was downregulated by WPBS (1% and 10%) relative to PGE2-only treatment, with efficacy comparable to or exceeding that of the positive control, ceramide 3 B (30 μM, p < 0.001). Statistical significance: ^### p < 0.001 vs. none; ** p < 0.01, *** p < 0.001 vs. PGE2-treated control.

Figure 6

RNA-seq analysis of the effect of WPBS treatment under inflammatory conditions. (A) Volcano plot of the changes in gene expression. Left: Inflammation (PGE2) vs. control (NC); several genes (red) upregulated by PGE2 (e.g., GDF15, IFITM1, and HMOX1) confirmed the induction of inflammation. Right: WPBS-treated (after PGE2) vs. PGE2-only; numerous pro-inflammatory genes (blue) were downregulated by WPBS (e.g., IL6, CXCL8, and C3). Dotted lines indicate significance thresholds (q-values < 0.05). (B) Heatmap of global gene expression (top 50 DEGs) shows distinct clustering of samples: WPBS-treated cells clustered separately from PGE2-only cells and closer to untreated controls. (C) GSEA of Hallmark pathways. Top: In PGE2 vs. control, inflammatory and stress pathways (“INTERFERON_ALPHA_RESPONSE,” “UV_RESPONSE_UP,” “INFLAMMATORY_RESPONSE”) were positively enriched in PGE2-treated cells. Bottom: In WPBS vs. PGE2, the same pathways (including “TNFA_SIGNALING_VIA_NFKB”) were negatively enriched with WPBS treatment (q-value < 0.05), indicating that WPBS suppressed these pathways.