Mycotoxin is a class of poisonous secondary metabolites generated by filamentous fungi and found in agricultural commodities worldwide. Therefore, the current study aimed to investigate how aflatoxin B1 affected hepatic cellular architecture and Matrix metalloproteinase expression in particular (MMP1 and MMP7) in the livers of experimental mice (IHC). A total of sixteen mice (four groups) were studied after being given pure aflatoxin B1 (9mg/kg B. W., 6mg/kg B. W., and 3mg/kg B. W. ) (produced from Aspergillus flavus) or a control group (not treated). MMP1 and MMP7 expressions were also measured using the MMP1 and MMP7 expression assays (IHC). The degree of liver damage is related to the AFB1 concentration and the duration of exposure. IHC reveals a considerable rise in MMP1 and MMP7 expression in the livers of mice given a maximum concentration of 90% ((9 mg/B. W. ) pure AFB1), which approached the toxin's effect toxic dosage. MMP1 and MMP7 expression were also increased by AFB1 at dosages of 60 and 30% (6mg/BW and 3mg/B. W., respectively), although not to the same extent as 90%. MMP1 was significantly more expressed than MMP7 compared to control, and AFB1 at 90, 60, and 30% concentrations caused changes in hepatic cellular architecture, organization, and liver tissue damage and dramatically increased MMP1 and MMP7 production in hepatic tissue following treatment. Increased levels of pure aflatoxin B1 will harm liver tissue and MMP1 and MMP7 expression. MMP1 was more substantially expressed than MMP7.

Aim: Due to weak diagnosis and treatment of PDAC, detection of PDAC possible biomarkers in early stage is the main aim of this study. Background: Pancreatic ductal adenocarcinoma (PDAC) is known as an exocrine cancer with a 5-year overall survival of 11%. Methods: Gene expression profiles of early stage of PDAC tissue and normal tissue are downloaded from gene expression omnibus (GEO) and evaluated via GEO2R. The significant differentially expressed genes (DEGs) are investigated via protein-protein interaction (PPI) network analysis and gene ontology. Results: Among 104 DEGs, ALB, COL1A1, COL1A2, MMP1, POSTN, PLAU, and COL3A1 were pointed out as hub nodes. “Gelatin degradation by MMP1, 2, 3, 7, 8, 9, 12, 13” group of 52 biological terms were identified as the main affected terms. Conclusion: In conclusion, ALB, MMP1, and COL1A1 genes were highlighted as possible biomarkers of early stage of PDAC. Dysfunction of extracellular matrix was identified as a main event in patients

Introduction: Hypertrophic scars (HSs) are the result of excessive collagen deposition at the wound area, which gives raised, pruritic, and erythematous lesions. Until now, there is no optimal treatment for abnormal scarring, including HSs. Because of the anti-inflammatory and anti-fibrotic effects of catechins, the aim of this work was to investigate the preventive potential of catechin hydrate (CH) against HS formation in rabbits. Methods: Topical CH ointments were prepared by the levigation method. 10 New Zealand White rabbits in 5 groups were used in this experimental research as follows: negative control, Eucerin (ointment base) treated group, and CH 1, 2, and 4% w/w ointment-treated groups. The anti-scarring effects of CH were investigated by measuring the epidermal thickness index (ETI), the scar elevation index (SEI), the amount of collagen deposition, the type І and type ІІІ collagen, and the MMP1 levels in scar tissue. Results: Our results showed that after treatment with topical CH, the scars formed in the wound site were almost normal and flattened to the surrounding skin level, while in the control and eucerin-treated groups, the scars were raised and had a darker color than normal skin. In addition, topical CH in all concentrations significantly (p<0.05) reduced ETI, SEI, the collagen deposition, and the levels of type І and type ІІІ collagen compared to the control group. Moreover, CH 4% significantly (p<0.05) enhanced the MMP1enzyme levels compared to the control group. Conclusion: Based on our findings, CH has the potential for the prevention of hypertrophic scar formation.