BACKGROUND: Alkali-burned corneas can seldom heal properly to restore corneal transparency. Treatment of this severe disorder of the ocular surface remains a challenge. AIM OF THE WORK: was to investigate whether systemically transplanted bone marrow mesenchymal stem cells (BM-MSCs) can promote corneal wound healing after alkali burn. MATERIAL AND METHODS: Thirty five male New Zealand rabbits were used in this study. The animals were divided into three groups. Group I; the control group was sham operated. Group II; corneal alkali burn was created. Group III; underwent corneal alkali burn then treated with BM-MSCs. All corneas were collected after fourteen and twenty eight days. Evaluation using H&E, PAS & alkaline phosphatase reaction was carried out. Immune histo-chemical staining for CD44 and vimentin was performed as well. RESULTS: the corneal epithelium of (Group II) showed marked alterations. Vascularization, cellular infiltration and irregularity of the collagen fibers were also seen in the substantia propria. Increase in the thickness of the Descemet's membrane was noticed as well. On the other hand, at the time of 28 days, Group III rabbits showed best histological results with nearly healed corneas compared to other groups. Meanwhile, vimentin was more strongly expressed in Group III assessing the differentiating ability of BM-MSCs. CONCLUSION: BM-MSCs could effectively promote corneal alkali burn healing.
Alkalies* ; Alkaline Phosphatase ; Animals ; Bone Marrow* ; Burns* ; Collagen ; Cornea ; Descemet Membrane ; Epithelium, Corneal ; Hand ; Humans ; Male ; Mesenchymal Stem Cell Transplantation* ; Mesenchymal Stromal Cells ; Rabbits ; Vimentin ; Wound Healing

Background/Aims: Ulcerative colitis (UC) is a chronic inflammatory disorder with indefinite etiology; however, environmental, genetic, immune factors and microbial agents could be implicated in its pathogenesis. UC treatment is lifelong, therefore; the potential side effects and cost of the therapy are significant. Yarrow is a promising medicinal plant with the ability to treat many disorders, owing to its bioactive compounds especially the essential oil. The main aim of this research was to investigate the therapeutic effect of the yarrow oil on colitis including the involved mechanism of action. Methods: In 21-female C57BL/6 mice were divided into 3 groups; control group, colitis model group, and oil-treated group. Groups 2 and 3 received 5% dextran sulfate sodium (DSS) in drinking water for 9 days, and concomitantly, only group 3 was given 100 mg/kg yarrow oil. Mice were examined for their body weight, stool consistency and bleeding, and the disease activity indexes were calculated. Results: Oral administration of yarrow oil markedly repressed the severity of UC via the reduction of the inflammatory signs and restoring colon length. The oil was able to down-regulate nuclear factor kappa light chain enhancer of activated B cells (NF-κB), up-regulate peroxisome proliferator-activated receptor gamma (PPAR-γ), and enhance transforming growth factor-β expression. The oil normalized the tumor necrosis factor-α expression, restored the normal serum level of interleukin-10 (IL-10) and reduced the serum level of IL-6. Conclusions Yarrow oil mitigated UC symptoms and regulated the inflammatory cytokines secretion via regulation of NF-κB and PPAR-γ pathways in the mice model, however, this recommendation requires further investigations using clinical studies to confirm the use of the oil on humans.

Background/Aims: Ulcerative colitis (UC) is a chronic inflammatory disorder with indefinite etiology; however, environmental, genetic, immune factors and microbial agents could be implicated in its pathogenesis. UC treatment is lifelong, therefore; the potential side effects and cost of the therapy are significant. Yarrow is a promising medicinal plant with the ability to treat many disorders, owing to its bioactive compounds especially the essential oil. The main aim of this research was to investigate the therapeutic effect of the yarrow oil on colitis including the involved mechanism of action. Methods: In 21-female C57BL/6 mice were divided into 3 groups; control group, colitis model group, and oil-treated group. Groups 2 and 3 received 5% dextran sulfate sodium (DSS) in drinking water for 9 days, and concomitantly, only group 3 was given 100 mg/kg yarrow oil. Mice were examined for their body weight, stool consistency and bleeding, and the disease activity indexes were calculated. Results: Oral administration of yarrow oil markedly repressed the severity of UC via the reduction of the inflammatory signs and restoring colon length. The oil was able to down-regulate nuclear factor kappa light chain enhancer of activated B cells (NF-κB), up-regulate peroxisome proliferator-activated receptor gamma (PPAR-γ), and enhance transforming growth factor-β expression. The oil normalized the tumor necrosis factor-α expression, restored the normal serum level of interleukin-10 (IL-10) and reduced the serum level of IL-6. Conclusions Yarrow oil mitigated UC symptoms and regulated the inflammatory cytokines secretion via regulation of NF-κB and PPAR-γ pathways in the mice model, however, this recommendation requires further investigations using clinical studies to confirm the use of the oil on humans.