Acetylsalicylic acid treatment reduce Fusarium rot development and neosolaniol accumulation in muskmelon fruit.

Fusarium rot of muskmelon is a common and frequently-occurring postharvest disease, which leads to quality deterioration and neosolaniol (NEO) contamination. New strategies to control postharvest decay and reduce NEO contamination are of paramount importance. The effects of acetylsalicylic acid (ASA) treatment on the growth of Fusarium sulphureum in vitro, and Fusarium rot development and NEO accumulation in fruits inoculated with F. sulphureum in vivo were investigated. The results showed that ASA inhibited the growth of F. sulphureum, evident morphological and major cellular changes were observed under the microscope. In vivo testing showed that 3.2 mg/mL ASA significantly suppressed Fusarium rot development and NEO accumulation after 6 and 8 d of pathogen inoculation. Meanwhile, Tri gene expressions involved in NEO biosynthesis were down-regulated after treatment. Taken together, ASA treatment not only reduced Fusarium rot development by inhibiting the growth of F. sulphureum, but decreased NEO accumulation by suppressing NEO biosynthesis pathway.

Effects of abnormal savda munzip on the proliferation activity and migration ability of fibroblasts derived from hypertrophic scar in vitro.

Background. To explore the effect of ASMq on proliferation and migration ability of the fibroblast derived from HS of donor (HSFbs) in vitro. Methods. The HSFbs were cultured from tissue specimens and passaged to the 3~4 generation, which were treated with the different concentrations of ASMq and 5-Fu from 1 to 11 days. The difference of HSFbs proliferation activity was analyzed by the CCK-8 method. The HSFbs migration ability in ASMq (0.4 mg/mL) was analyzed by the Cell Scratch method. Results. Transmission electron microscope result shows ASMq concentration significantly increases and fibroblast cell structure markedly change in the experimental group. The proliferation activity of the HSFbs was obviously weakened in ASMq groups than those of the group A (P < 0.05) at seven days. The group C (0.4 mg/mL) is better suitable than other three ASMq treatment groups. Cell Migration Assay shows that the migration ability HSFbs was significantly reduced in ASMq (0.4 mg/mL) treatment group compared with those of blank control group at both 24 h and 48 h (P < 0.05). Conclusions. These results suggest that ASMq effectively restrains the proliferation and migration ability of the HTSFbs in vitro, which can be one of the mechanisms for the prevention and treatment of HS.

Effect of Abnormal Savda Munziq on hypertrophic scar formation in a rabbit ear model.

OBJECTIVE: To investigate whether administrating Abnormal Savda Munziq (ASMq), a traditional Uighur herbal preparation used for the prevention or treatment of diseases, affects hypertrophic scar (HTS) formation by using an established rabbit ear model. METHODS: The HTS rabbit model was created by circular fullthickness skin excisions on both ears of rabbits. Twenty rabbits were randomized into four groups, with 5 rabbits and 60 wounds in each group. Group A was the control group, treated with normal saline daily. Groups B, C, and D were the treatment groups at three different doses of ASMq (400, 800, and 1200 mg/kg body weight, respectively, daily, by gastrogavage). Twenty wounds were randomly chosen from each group on the 40th day after treatment and specimen were examined. Scar elevation index (SEI) was analyzed with histological assessment, and ultrastructure analysis was analyzed with a transmission electron microscopy. RESULTS: Groups B, C, and D demonstrated significant reductions in SEI as compared with the control group at 35.9% (P=0.0212), 48.2% (P=0.0108), and 52.7% (P=0.0103), respectively in a dose-response manner. SEI was lowered in Group D compared with Group B with a significant difference (P=0.015). However, there were no significant differences between Groups B and C, or between Groups C and D. Histological analysis showed that highdose ASMq (1200 mg/kg) could enhance the softening of HTS of rabbit ears and increase the compliance as shown in general. Ultrastructure analysis showed that with increased ASMq dose, the fibroblasts, pro-collagen, collagen, endoplasmic reticulum and ribosomes were reduced gradually. CONCLUSIONS: Orally administered ASMq significantly reduces the severity of HTS in the rabbit ear model. The findings of this study may have clinical implications on the management of human HTS.

[Effect of uighur medicine abnormal savda munzip on human hypertrophic scar fibroblasts in vitro].

OBJECTIVE: To evaluate in vitro effect of abnormal savda munziq (ASMq) on the proliferation and apoptosis of human hypertrophic scar fibroblasts (HSFs). METHODS: HSFs were divided into six groups to receive different treatments as group A (blank control group), group B-E (ASMq in different concentration), and group F(5-Fu). Each group contains six specimens. The HSFs were cultured in vitro. After culture for 48 hours, the CCK8 test and flow cytometry methods were used to detect the proliferation, cell cycle and apoptosis. RESULTS: The proliferation of HSFs in the B, C, D and E groups was inhibited at G2/M period, while it was inhibited at G0/S period in group F (P < 0.05). The inhibition effect of ASMq (0.1-1.0 mg/ml) on the fibroblasts enhanced in a concentration-dependent manner. Flow cytometry analysis with annexin V-FITC and PI staining confirmed the apoptotic. When HSFs were exposed to ASMq at 1.0 mg/ml (group E) for 48 h, the percentage of apoptotic cells increased to (43.7 +/- 2.58)%, which was significantly higher than that of blank control group (2.2 +/- 0.59)%. The induced apoptosis effect was also increased in a concentration-dependent manner. CONCLUSION: ASMq has a inhibitory effect on the proliferation and an enhancement effect on the apoptosis of fibroblast. ASMq could be used as an effective drug for treatment of hypertrophic scar.