[The Preliminary Study on Anti-photodamaged Effect of Astaxanthin Liposomes in Mice Skin].

OBJECTIVE: To study the protective effects of astaxanthin liposome (Asx-lipo) on photodamage by UVB in mice skin. METHODS: 40 C57BL/6J mice were randomly divided into four groups: The blank group (no irradiation, no drug use), model group (UVB light injury group, no drug use), control group (irradiation + astaxanthin), experimental group (irradiation + astaxanthin liposome), each group with 10 mice. Each group was given the corresponding light (the radiation intensity was 2 mW·cm2, the time of irradiation was 60 s, 1 times a day for the first 5 days, and 1 times every other day for the next 9 days, 10 times in a total of 2 weeks.) and drug intervention (topically treated with 4 mL 0.2‰ astaxanthin or 4 mL 0.2‰ Asx-lipo 10 min before the irradiation) for two weeks. After that, samples were examined by the following indicators: the histological changes of skin, Ki-67, 8-hydroxy-2'-deoxyguanosine(8-OHdG), superoxide dismutase(SOD) activities and serum matrix metalloproteinase-13 (MMP-13). RESULTS: HE staining the model group and the control group showed that the dermis became thin, the dermal collagen fibers were long and thin, and the arrangement was loose and disordered. Compared with the blank group, the expression of Ki-67, MMP-13 and 8-OHdG increased and SOD activity decreased, and the differences were statistically significant (P<0.05). Compared with the model group, the pathological changes of skin tissues in the experimental group were significantly improved, with decreased expressions of Ki-67, MMP-13 and 8-OHdG and increased SOD activity, and the differences were statistically significant (P<0.05). CONCLUSION: The photodamage of mice skin can be improved by topical Asx-lipo. The mechanism may be related to the strong antioxidation of Asx-lipo.

A Case of Neuropsychiatric Systemic Lupus Erythematosus With Hair Loss as the First Diagnostic Symptom.

Neuropsychiatric systemic lupus erythematosus is a serious complication of systemic lupus erythematosus. A 33-year-old female patient had repeated hair loss for more than 3 years. A dermatologic examination showed several pieces of irregularly shaped hair loss patterns in the center of the patient's scalp. The systemic treatment included oral hydroxychloroquine, aspirin enteric-coated tablets and prednisone, and intrathecal injection of dexamethasone and methotrexate. The local treatment included intralesional injection of triamcinolone acetonide and lidocaine in the lesion area, 0.1% tacrolimus ointment for external use. After 2-month treatment, hair regrew in a non-scarring patchy alopecia region with no further hair loss.

Two novel mutations on exon 8 and intron 65 of COL7A1 gene in two Chinese brothers result in recessive dystrophic epidermolysis bullosa.

Dystrophic epidermolysis bullosa is an inherited bullous dermatosis caused by the COL7A1 gene mutation in autosomal dominant or recessive mode. COL7A1 gene encodes type VII collagen - the main component of the anchoring fibrils at the dermal-epidermal junction. Besides the 730 mutations reported, we identified two novel COL7A1 gene mutations in a Chinese family, which caused recessive dystrophic epidermolysis bullosa (RDEB). The diagnosis was established histopathologically and ultrastructurally. After genomic DNA extraction from the peripheral blood sample of all subjects (5 pedigree members and 136 unrelated control individuals), COL7A1 gene screening was performed by polymerase chain reaction amplification and direct DNA sequencing of the whole coding exons and flanking intronic regions. Genetic analysis of the COL7A1 gene in affected individuals revealed compound heterozygotes with identical novel mutations. The maternal mutation is a 2-bp deletion at exon 8 (c.1006_1007delCA), leading to a subsequent reading frame-shift and producing a premature termination codon located 48 amino acids downstream in exon 9 (p.Q336EfsX48), consequently resulting in the truncation of 2561 amino acids downstream. This was only present in two affected brothers, but not in the other unaffected family members. The paternal mutation is a 1-bp deletion occurring at the first base of intron 65 (c.IVS5568+1delG) that deductively changes the strongly conserved GT dinucleotide at the 5' donor splice site, results in subsequent reading-through into intron 65, and creates a stop codon immediately following the amino acids encoded by exon 65 (GTAA→TAA). This is predicted to produce a truncated protein lacking of 1089 C-terminal amino acids downstream. The latter mutation was found in all family members except one of the two unaffected sisters. Both mutations were observed concurrently only in the two affected brothers. Neither mutation was discovered in 136 unrelated Chinese control individuals. This study reveals novel disease-causing mutations in the COL7A1 gene.