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Keloids are benign tumors that originate from scar tissues, but they usually overgrow beyond the original wounds. In a three-month single-center clinical trial, 69 patients were randomly divided into three groups. Patients in group 1 were treated with intralesional injection of diprospan (2 mg betamethasone disodium phosphate and 5 mg betamethasone dipropionate in 1 ml) with one-month intervals for three months. Patients in groups 2 and 3 were injected with a combination of 0.5 ml 5-fluorouracil (5-FU; 25 mg/ml) and diprospan as above for three months also. Prior to each injection, the keloids of patients in group 3 were additionally irradiated by a 1,064-nm neodymium-yttrium-aluminum-garnet (Nd:YAG) laser with a single pulse at an energy density of 90-100 J/cm 2 and a pulse width of 12 msec. Clinical responses were evaluated by patient self-assessment and overall assessment by an observer according to the clinical signs of erythema, pruritus and pliability. A total of sixty-two patients completed the tests of the present study. At 2 and 3 months, the patients in all treatment groups showed an acceptable improvement in nearly all measurements. At the end of the study, the erythema and toughness score was significantly reduced and itch reduction was significantly greater in the diprospan + 5-FU + Nd:YAG group when compared to those in the other groups (P<0.05 for all indexes). The acceptable responses (good to excellent improvements) reported by blinded observers were as follows: 12% in the diprospan group, 48% in the diprospan + 5-FU group and 69% in the diprospan + 5-FU + Nd:YAG group. All of the results indicated that the combination of diprospan + 5-FU + Nd:YAG was the most efficacious therapy for keloid scars.

The aim of this study was to investigate the photoprotective and immunoregulatory capacities of ginsenoside Rg1 in skin irradiated by chronic ultraviolet B (UVB) and to verify the potential mechanisms of action. BALB/c mice were pretreated with a topical application of ginsenoside Rg1 and irradiated with different doses of UVB daily for 30 consecutive days. Following chronic UVB irradiation, there were significant pathological changes in the skin of the BALB/c mice, including hyperkeratosis, acanthosis, sponge-like edematization and sunburn occurring in the epidermis, while edema, telangiectasis and inflammatory cell infiltration were observed in the papillary layer of the dermis. Treatment with ginsenoside Rg1 was able to reduce such changes induced by UVB irradiation. The number of p53 protein-positive stained cells following UVB irradiation was also observed by immunohistochemical analysis. Ginsenoside Rg1 downregulated the p53 protein expression induced by UVB irradiation, leading to reductions of 69.50, 23.53 and 12.93% at doses of 30, 60 and 120 mJ/cm 2 , respectively. Using reverse transcription polymerase chain reaction (RT-PCR), reductions in the levels of interferon (IFN)-γ mRNA expression were detected following UVB exposure; reductions of 19.6, 36.3 and 39.6% were observed following UVB irradiation at doses of 30, 60 and 120 mJ/cm 2 , respectively. The interleukin (IL)-10 mRNA expression levels increased by 40.1, 71.0 and 89.4% and the tumor necrosis factor (TNF)-α mRNA expression levels increased by 36.4, 18.4 and 8.6% following UVB irradiation at doses of 30, 60 and 120 mJ/cm 2 , respectively. However, pretreatment with ginsenoside Rg1 was observed to markedly attenuate the UVB irradiation-induced effects on the mRNA expression levels of the three cytokines. The topical application of ginsenoside Rg1 was able to protect the irradiated skin from UVB injury and reduce UVB-induced p53 protein expression. Ginsenoside Rg1 also demonstrated a potential regulatory effect on the UVB-induced local expression of the mRNA of the cytokines IFN-γ, IL-10 and TNF-α, which may be important in its immunoregulatory and inflammatory mechanisms.