Background and aim: Fractional CO₂ laser is therapeutic for acne atrophic scar, but its effect usually is limited after multiple sessions, with occasional adverse reactions. This study aimed to evaluate the efficacy and safety of a new modality combining ultra-pulse CO₂ laser and fractional CO₂ laser (multiple mode procedures [MMP]) in the treatment of acne atrophic scars. Method: From December 2017 to January 2023, a total of 103 patients with facial acne atrophic scars treated with MMP technique were retrospectively analyzed. MMP was performed for 1–4 sessions with an interval of approximately three months. Based on photographs taken before and after treatment, overall atrophic scar improvement was assessed according to the ECCA grading scale, the modified Manchester Scar Scale and the 4-point Global Assessment Scale (GAS). The safety was evaluated by the degree of pain during treatment and postoperative adverse reactions. Results: All the 103 patients received treatment and completed follow-up, with an average of two sessions. The mean ECCA score decreased from 162.7 to 93.1 with statistically significant difference (p < 0.001). The mean GAS score increased by an average of 2.3 ± 0.9. The GAS improvement more evident for “boxcar” atrophic scars (2.7 ± 0.8) than for “rolling” (2.3 ± 0.8) and “icepick” scars (1.7 ± 0.8) (p < 0.001). The average improvement scores for color, distortion and texture were 2.0 ± 0.9, 2.2 ± 0.9 and 2.3 ± 0.8, respectively. The mean pain score during treatment was 3.9 ± 0.8, and the mean duration of erythema was 30.7 ± 3.5 days. Only three patients developed hyperpigmentation at the treated site within a few months. Discussion: Ultra-pulse CO₂ fractional laser MMP technique can effectively improve the condition of facial atrophic acne scars with limited adverse reactions.

Low‐dose 5‐aminolevulinic acid photodynamic therapy (ALA‐PDT) has been used to cope with skin photoaging, and is thought to involve DNA damage repair responses. However, it is still unknown how low‐dose ALA‐PDT regulates DNA damage repair to curb skin photoaging. We established a photoaging model using human dermal fibroblasts (HDFs) and rat skin. RNA‐sequencing (RNA‐seq) analysis was conducted to identify differentially expressed genes (DEGs) in HDFs before and after low‐dose ALA‐PDT treatment, followed by bioinformatics analysis. Senescence‐associated β‐galactosidase (SA‐β‐gal) staining was employed to assess skin aging‐related manifestations and Western blotting to evaluate the expression of associated proteins. A comet assay was used to detect cellular DNA damage, while immunofluorescence to examine the expression of 8‐hydroxy‐2′‐deoxyguanosine (8‐oxo‐dG) in cells and skin tissues. In both in vivo and in vitro models, low‐dose ALA‐PDT alleviated the manifestations of ultraviolet B (UVB)‐induced skin photoaging. Low‐dose ALA‐PDT significantly reduced DNA damage in photoaged HDFs. Furthermore, low‐dose ALA‐PDT accelerated the clearance of the photoproduct 8‐oxo‐dG in photoaged HDFs and superficial dermis of photoaged rat skin. RNA‐seq analysis suggested that low‐dose ALA‐PDT upregulated the expression of key genes in the base excision repair (BER) pathway. Further functional validation showed that inhibition on BER expression by using UPF1069 significantly suppressed SA‐β‐gal activity, G2/M phase ratio, expression of aging‐associated proteins P16, P21, P53, and MUTYH proteins, as well as clearance of the photoproduct 8‐oxo‐dG in photoaged HDFs. Low‐dose ALA‐PDT exerts anti‐photoaging effects by activating the BER signalling pathway.

To evaluate the photoprotective effect of 5-aminolaevulinic acid-based photodynamic therapy (ALA-PDT) on ultraviolet B (UVB)-induced skin photodamage. In vivo experiments, the dorsal skin of hairless mice were treated with ALA-PDT or saline-PDT, and then exposed to 180 mJ/m² UVB. Results showed that the number of sunburn cells and apoptotic cells in the epidermis of ALA-PDT-treated groups at 24 h after UVB irradiation were significantly decreased compared with those in the UVB groups. And the removal rate of CPDs was obviously higher in ALA-PDT-treated groups. At 48 h, the number of Ki67 positive nuclei in ALA-PDT-UVB group was significantly fewer than that in UVB group. Further in vitro experiments, human keratinocyte cell line (HaCaT) cells of two groups (one treated with ALA-PDT, the other untreated), were exposed to 60 mJ/m² UVB irradiation. We found 0.5 mmol/L of ALA and 3 J/cm² of red light did not affect the vitality of cells, and could reduce UVB induced apoptosis, accelerate the clearance of CPDs, inhibit proliferation and activate p53. Thus, our data demonstrate that ALA-PDT pretreatment can induce a protective DNA damage response that protects skin cells from UVB-induced photodamages.

Background and Aim: Keloids cannot be effectively treated using monotherapy regimens. This study aimed to evaluate the efficacy and safety of ablation (a novel needle‐assisted electrocoagulation technique) combined with pharmacotherapy (corticosteroid and 5‐fluorouracil [5‐FU] injections) in removing keloids and to investigate the underlying biological mechanisms.Methods: The effects of energy consumption and duration of needle‐assisted electrocoagulation on the ablation zone were tested in porcine liver tissue, which simulates human skin. The regulatory effects of ablation combined with pharmacotherapy on collagen deposition, cell proliferation, and angiogenesis were analyzed in a keloid‐bearing nude mouse model in vivo. In a clinical trial involving six patients with keloids, the Vancouver Scar Scale (VSS) and Patient and Observer Scar Assessment Scale (POSAS) scores were graded before treatment and 1 month after one cycle of ablation combined with corticosteroid and 5‐FU therapy.Results: Higher energy consumption and longer duration of electrocoagulation resulted in a larger ablation zone and higher surface temperature. Ablation combined with pharmacotherapy significantly reduced keloid volume in nude mice, upregulated MMP‐1 and MMP‐3, downregulated COL I and COL III, and inhibited angiogenesis and proliferation. This combination also significantly reduced the VSS and POSAS scores in patients with keloids after treatment without any obvious adverse events.Conclusion: Our findings show that electroablation combined with pharmacotherapy effectively reduces keloid volume by inhibiting collagen deposition, angiogenesis, and cell proliferation. Thus, this novel combination may serve as a safe therapeutic approach for keloid removal.