Decrease In Inflammatory Cells Research Articles

Role of Dexamethasone on immune dysregulation mediated through Th1/Th2 cytokine balance in mice challenged with type 1 diabetes and allergic asthma

Dysregulated equilibrium between T helper 1 (Th1) and T helper 2 (Th2) immune responses has been implicated in the pathogenesis of type 1 diabetes (T1D) and asthma. Conflicting evidence exist explaining the association between T1D and asthma and is still a point of debate. In the present study, our objective was to investigate the influence of associated T1Dco morbid condition on the induction of experimental asthma in mice and also to evaluate the efficacy of Dexamethasone (0.5 mg/kg, s.c.ly) in these mice. Type 1 diabetes was induced by a single intravenous injection of alloxan (80 mg/kg) in Balb/c mice. Following diabetes induction, mice were sensitized with an intraperitoneal injection of 50 µg ovalbumin (Ova) emulsified in 2.5 mg aluminum hydroxide on days 3 and 8. From day 13 to day 15, animals were challenged intranasally with 100 µg Ova in 25 µl of sterile saline. Dexamethasone treatment was initiated on sensitization day and continued once in 2 days thereafter until day 15. Control animals received only saline without Ova. On day 16, mice were subjected to nasal hyperresponsiveness (NHR) immediately after the Ova challenge. Bronchioalveolar lavage fluid (BALF), blood, and lungs were collected 1h post completion of NHR for further analysis. Alloxan diabetic mice showed significantly lower levels of eosinophils in BALF and blood with the corresponding decrease in inflammatory cells around airways in hematoxylin & eosin-stained lung sections, but with no change in NHR than in non-diabetics after Ova sensitization and challenge. Dexamethasone treatment showed a significant reduction of airway inflammation and related Th2 immune responses, with a lesser magnitude of efficacy in diabetic asthma mice than in non-diabetic asthma mice. The presence of T1D featured a unique, yet the intermediary stage of asthma induction and also presented an altered magnitude of Dexamethasone efficacy compared to the absence of T1D in the murine model of Ova induced asthma.

Wound healing property of milk in full thickness wound model of rabbit

ObjectiveWound healing consists of several continuous phases in which various cells and chemical intermediates are involved. Milk as a rich source of nutritional elements has proved to have potential benefits for treatment of various diseases. The present study was designed to investigate the healing effect of low-fat cow's milk on an open skin wound model in the rabbit. MethodsThe 2%, 5%, and 10% (w/w) ointments of lyophilized powder of low-fat milk were prepared in the eucerin base and were applied twice daily in the treatment groups. Phenytoin 1% ointment was used as a standard control. The healing effect of the milk ointment (MO) was evaluated through the measurement of wound surface area, the extent of tissue tension, and the content of hydroxyproline. Histological evaluation of skin tissue specimens was also performed using hematoxylin and eosin staining. ResultsThe results showed that the healing rate in the treatment group was significantly higher than that of untreated group and eucerin group (p < 0.01). The best healing effect was seen in 5% milk ointment with the shortest healing time (15 days) and the highest tissue tension in comparison to other groups. Although the tissue hydroxyproline content in this group was slightly lower than that of the phenytoin group, this difference was not significant. Histologic, findings indicated increased collagen fibers, increased fibroblasts and an evident decrease in inflammatory cells in that group. ConclusionIt can, therefore, be concluded that low-fat cow's milk has significant beneficial effects on skin wound healing. Therefore, it may be used as a healing agent in different types of the wound in humans after certain clinical trials.

Cefquinome-loaded microsphere formulations against Klebsiella pneumonia infection during experimental infections

The aim of this study was to prepare cefquinome-loaded polylactic acid microspheres and to evaluate their in vitro and in vivo characteristics and pharmacodynamics for the therapy of pneumonia in a rat model. Microspheres were prepared using a 0.7 mm two-fluid nozzle spray drier in one step resulting in spherical and smooth microspheres of uniform size (9.8 ± 3.6 μm). The encapsulation efficiency and drug loading of cefquinome were 91.6 ± 2.6% and 18.7 ± 1.2%, respectively. In vitro release of cefquinome from the microspheres was sustained for 36 h. Cefquinome-loaded polylactic acid microspheres as a drug delivery system was successful for clearing experimental Klebsiella pneumonia lung infections. A decrease in inflammatory cells and an inhibition of inflammatory cytokines TNF-α, IL-1β and IL-8 after microspheres treatment was found. Changes in cytokine levels and types are secondary manifestations of drug bactericidal effects. Rats were considered to be microbiologically cured because the bacterial load was less than 100 CFU/g. These results also indicated that the spray-drying method of loading therapeutic drug into polylactic acid microspheres is a straightforward and safe method for lung-targeting therapy in animals.

Wound healing activity of Streptocaulon juventas root ethanolic extract.

Streptocaulon juventas is a well-known plant that has antimicrobial activity, in vitro antiplasmodial activity, anti-proliferative activity, and antioxidant activity. In this study, we showed experimental evidence that proved that S. juventas root ethanolic extract has wound healing activities. First, in a mouse excision wound model, S. juventas root ethanolic extract at a dose of 100 mg/kg/day significantly reduced the wound closure time. After 7 days, the wound granulation tissue in mice treated with the extract exhibited a 2.3-fold decrease in inflammatory cells, a 1.7-fold increase in fibroblasts and enhanced angiogenesis. Molecular analysis also revealed that after wounds were treated with S. juventas root ethanolic extract, TNF-α and NF-κB1 gene expression were down-regulated by 4.7 and 3.7 times, respectively. In contrast, TGF-β1 and VEGF gene expression were up-regulated by 1.9 and 6.5 times, respectively. Taken together, our experimental data strongly show that the ethanolic extract from S. juventas root displays remarkable wound healing activity.

ID: 1072 Increasing dose of intravenous human adipose-derived stem cells improves the pancreatic function of diabetic mice

Mesenchymal tem cell transplantation is a novel treatment for diabetes mellitus, especially type 1 diabetes. Many publications have proved the effect of MSC therapy on reducing blood glucose and improving insulin production in type 1 diabetic animal as well as in clinic trials. However, there is no conclusion that how many cells are effective for diabetes. Thus, this study has investigated that different adipose-derived MSC doses affected glucose metabolism in diabetic mice. STZ-induced diabetic mice were intravenous transfused with human MSCs with dose either 106 (treated group A) or 2x106 cells/mouse (treated group B). Both treated and untreated mice were monitored the blood glucose levels, glucose and insulin tolerance test, pancreatic structure change and insulin production every week until 56 days after transplantation. The results showed that the higher dose of MSC could reduce death rate (66% vs. 0% death in group A vs. group B after 56 days of treatment, respectively) and remarkably lower blood glucose levels while the mice treated with 1x106 cells/dose remaining hyperglycemia. Moreover, the glucose tolerance and insulin tolerance as well as insulin production were improved in group B at 28 days after transplantation. The histochemical imaging further demonstrated the decrease of inflammatory cells in the islets and the restoration of pancreatic structures in higher-dose-MSCs-treated mice. Thus, the dose 2x106 cells of MSCs may be an effective strategy for diabetes mellitus concerning hyperglycemia, impaired glucose metabolism and islet destruction.

Evaluation of the Anti-Inflammatory Effect of Locally Delivered Vitamin C in the Treatment of Persistent Gingival Inflammation: Clinical and Histopathological Study.

Objective. The purpose of this study is to investigate the role and efficiency of the locally injected vitamin C in the treatment of persistent gingival inflammation. Design. Twenty adult patients with persistent chronic gingival inflammation were included in this study. The same dose of sterile vitamin C was injected in gingival tissues after the completion of phase I therapy. Gingival biopsies were taken after total resolution of inflammation. The specimens were examined histologically, using H&E stain. Results. Clinical evaluation revealed great improvement of the injected sites with recall visits. Histopathological results revealed marked decrease in inflammatory cells and epithelial thickness and a higher number of newly formed subbasal capillaries. Conclusions. Vitamin C is an effective adjunctive treatment in reducing various degrees of chronic gingival inflammation.

Nintedanib Ameliorates Lipopolysaccharide-Induced Pulmonary Fibrosis after Acute Respiratory Distress Syndrome through Suppression of VEGF/PDGF/FGF

Pulmonary fibrosis after acute respiratory distress syndrome (ARDS) is fatal disease. This study aimed to investigate the effect of nintedanib treatment on lipopolysaccharide (LPS)-induced mouse lung fibrosis after ARDS In vitro and in vivo. In vitro, nintedanib effectively inhibited the expression of both TGF-β1 and α-SMA after the LPS treatment in mouse lung fibroblasts. In vivo, nintedanib administrations at both early and late stages after LPS challenging protected the mice from lung fibrosis. First, nintedanib treatment resulted in a dramatic decrease in inflammatory cells in BAL fluid. Second, compared to the untreated mice with server lung fibrosis after LPS-induced ARDS, nintedanib treatment significantly reduced the levels of both lung tissue damage and collagen deposition. Third, nintedanib administration, both early and late stages, caused a decrease in Hyp contents and reduced α-SMA and I type collagen expression in the lung of C57BL/6 mice. These results suggest that nintedanib inhibits the transformation of LPS-induced fibroblasts into myofibroblasts in vitro and it ameliorates lung fibrosis in mice after LPS-induced ARDS.

Lysosomal pH Decrease in Inflammatory Cells Used To Enable Activatable Imaging of Inflammation with a Sialic Acid Conjugated Profluorophore.

Inflammation causes significant morbidity and mortality, necessitating effective in vivo imaging of inflammation. Prior approaches often rely on combination of optical agents with entities specific for proteinaceous biomarkers overexpressed in inflammatory tissues. We herein report a fundamentally new approach to image inflammation by targeting lysosomes undergoing acidification in inflammatory cells with a sialic acid (Sia) conjugated near-infrared profluorophore (pNIR). Sia-pNIR contains a sialic acid domain for in vivo targeting of inflamed tissues and a pNIR domain which isomerizes into fluorescent and optoacoustic species in acidic lysosomes. Sia-pNIR displays high inflammation-to-healthy tissue signal contrasts in mice treated with Escherichia coli, Staphylococcus aureus, or lipopolysaccharide. In addition, inflammation-associated fluorescence is switched off upon antibiotics treatment in mice. This report shows the potentials of Sia-pNIR for activatable dual-modality inflammation imaging, and particularly the use of lysosomes of inflamed cells as a previously unappreciated biomarker for inflammation imaging.

Development of an immunomodulatory biomaterial: Using resolvin D1 to modulate inflammation

In our search for immunomodulatory biomaterials capable of modulating the inflammatory response through M2 macrophage polarization, we report here on a new strategy that resulted from the incorporation of resolvin D1 (RvD1), a pro-resolution lipid mediator in porous 3D chitosan (Ch) scaffolds, followed by its lyophilisation. We have investigated the inflammatory response caused by this biomaterial in vivo using a mouse air-pouch model of inflammation. We found that this developed material caused a decrease in inflammatory cells recruited to the implant site, together with higher numbers of F4/80+/CD206+ cells (M2 macrophages) and lower numbers of F4/80+/CCR7+ cells (M1 macrophages). It also induced a general decrease in pro-inflammatory cytokines, and caused a decrease in the inflammatory cells observed around and within the implanted scaffolds, when compared with Ch alone or Ch not submitted to lyophilisation after RvD1 incorporation. Our results demonstrate that we were able to develop an immunomodulating biomaterial that triggers a shift in the macrophage response towards a M2 reparative response that will be advantageous for the host.

Modulation of the inflammatory response to chitosan through M2 macrophage polarization using pro-resolution mediators

Tissue engineering and regenerative medicine have created a demand for biomaterials with specific functions such as the ability to modify the host immune response. The objective of this study was to evaluate the effect of two different pro-resolution lipid mediators, lipoxin A4 (LxA4) and resolvin D1 (RvD1), in the modulation of the inflammatory response to biomaterials through M2 macrophage polarization. This was investigated in vivo using a mouse air-pouch model of inflammation. Our results demonstrated that both LxA4 and RvD1 are able to shift the macrophage response to implanted Ch scaffolds to an M2 reparative response. The injection of these pro-resolution mediators caused a decrease in inflammatory cells recruited to the implant site together with higher numbers of F4/80+/CD206+ cells (M2 macrophages) and lower numbers of F4/80+/CCR7+ cells (M1 macrophages); it also induced a general decrease in several pro-inflammatory cytokines; and caused a significant decrease in the thickness and area of the fibrous capsule formed around the implanted scaffolds. In conclusion, the use of either LxA4 or RvD1 allowed the in vivo control of macrophage phenotypic profile and thus may play a significant role in regenerative medicine applications, namely through modulation of the inflammatory response.

Effects of low-power light therapy on wound healing: LASER x LED.

Several studies demonstrate the benefits of low-power light therapy on wound healing. However, the use of LED as a therapeutic resource remains controversial. There are questions regarding the equality or not of biological effects promoted by LED and LASER. One objective of this review was to determine the biological effects that support the use of LED on wound healing. Another objective was to identify LED´s parameters for the treatment of wounds. The biological effects and parameters of LED will be compared to those of LASER. Literature was obtained from online databases such as Medline, PubMed, Science Direct and Scielo. The search was restricted to studies published in English and Portuguese from 1992 to 2012. Sixty-eight studies in vitro and in animals were analyzed. LED and LASER promote similar biological effects, such as decrease of inflammatory cells, increased fibroblast proliferation, stimulation of angiogenesis, granulation tissue formation and increased synthesis of collagen. The irradiation parameters are also similar between LED and LASER. The biological effects are dependent on irradiation parameters, mainly wavelength and dose. This review elucidates the importance of defining parameters for the use of light devices.

Fasudil Ameliorates Disease Progression in Experimental Autoimmune Encephalomyelitis, Acting Possibly Through Antiinflammatory Effect

The purpose of this investigation was to further explore the mechanism(s) underlying the amelioration in EAE caused by Fasudil, particularly focusing on anti-inflammatory effect. We induced a chronic-progressive experimental autoimmune encephalomyelitis (EAE) in B6 mice immunized with myelin oligodendrocyte glycoprotein(35-55) and performed Fasudil intervention in early and late stages of the disease. The administration of Fasudil (40mg/kg, i.p) had a therapeutic effect in delaying the onset and ameliorating the severity of EAE, accompanied by the improvement in myelination and the decrease in inflammatory cells in spinal cords. Fasudil inhibited TLR-4, p-NF-kB/p65, and inflammatory cytokines (IL-1β, IL-6, and TNF-α) and enhanced IL-10 production in spinal cords. The ratio of arginase/iNOS was enhanced mainly in the spinal cords of EAE mice treated with Fasudil, reflecting a shift toward the M2 (antiinflammation) macrophage/microglia phenotype. The administration of Fasudil also induced the upregulation of CB2 receptor in spinal cords, but did not significantly trigger CB1 receptor. Levels of neurotrophic factors NGF, BDNF, and GDNF in the CNS were not altered by Fasudil. Fasudil ameliorates disease progression in EAE, acting possibly through antiinflammatory pathway.

Clinical course of drug-induced collagenous colitis and histological changes after drug withdrawal in a Japanese case series

Although the incidence of drug-induced collagenous colitis has been increasing, details of its clinical course and histological changes after withdrawal of the suspected causative drugs remain unclear. To shed light on this issue, we studied 15 patients with collagenous colitis diagnosed between 1999 and 2011 in our hospital. Clinical cure was achieved in 14 patients after withdrawal of the suspected causative drugs and in one patient after the administration of prednisolone. Six patients underwent a second colorectal endoscopic examination after clinical cure, and the histological features were compared with those in patients during the clinically active phase. Four of these six patients showed disappearance of the collagen band and a decrease in inflammatory cells, but the collagen band remained in the other two despite a decrease in inflammatory cells. Cell proliferation as shown by Ki-67 immunostaining was restored to normal, irrespective of whether the collagen band was retained. The surface-absorptive epithelia became mature in all patients. Histological improvement in collagenous colitis is believed to involve normalization of cell proliferation and maturation of the absorptive epithelium, and not necessarily disappearance of the collagen band.

Anthraquinone derivative O,O′-bis-(3′-iodopropyl)-1,4-dihidroxyanthraquinone modulates immune response and improves experimental autoimmune encephalomyelitis

The present study investigated the effects of the anthraquinone derivative (O,O′-bis-(3′-iodopropyl)-1,4-dihidroxyanthraquinone — DIPDHAQ), mitoxantrone analog, in an experimental autoimmune encephalomyelitis (EAE) model. The results showed that DIPDHAQ treatment improved the clinical signs of the disease (n=10; vehicle: 3.8±0.3; DIPDHAQ: 1.4±0.9). The improvement was associated with a decrease of inflammatory cells, demyelination, IL-17, IFN-γ, IL-12p40, IL-6, TGF-β, CCL5 and CCL20 levels in the spinal cord. DIPDHAQ presented a low cytotoxicity when in vitro assays were performed. Therefore, the findings suggest a major role for DIPDHAQ in multiple sclerosis, disease characterized as an autoimmune inflammatory disorder against myelin proteins of the brain and spinal cord. The attenuation of inflammation and consequently improvement of clinical signs, involving a decrease of pro-inflammatory cytokines and the low cytotoxicity of DIPDHAQ, suggest that this compound could be used as an alternative treatment for autoimmune diseases in the central nervous system.

Ameliorative effect of Aegle marmelos leaf extract on early stage alloxan-induced diabetic cardiomyopathy in rats

Objective: The pathogenesis of diabetic cardiomyopathy (DCM) is complex, and the therapeutic options available to treat DCM are limited. The present study was designed to investigate the effect of Aegle marmelos (L.) Correa (Rutaceae) leaf extract on early stage DCM in alloxan-induced diabetic rats.Methods: Diabetes was induced in Wistar rats (150–200 g) by injecting alloxan (150 mg kg−1; i.p.). Ethanol extract of A. marmelos leaves was administered at varying doses (100, 200, and 400 mg kg−1) and tolbutamide (100 mg kg−1) as standard. Fasting blood glucose (FBG), total cholesterol, thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), lactate dehydrogenase (LDH) and creatine kinase (CK) were determined by standard methods.Results: A. marmelos extract (AME) was found to decrease the levels of FBG, total cholesterol, TBARS, LDH and CK, and increase the levels of GSH, CAT and SOD dose dependently as compared to diabetic control groups. The maximum dose-dependent decrease in TBARS (63.46%), LDH (34.04%), CK (53.14%), and increase in GSH (64.91%), CAT (59.34%), SOD (69.65%) was evident at an optimum dose of 200 mg kg−1. Histopathological studies revealed salvage in the morphological derangements as indicated by absence of necrosis and marked decrease in inflammatory cells in AME-treated groups as compared to diabetic control.Conclusions: The present investigations conclude that treatment with AME attenuates the severity and improves the myocardium in the early stages of alloxan-induced DCM at a dose of 200 mg kg−1.

Attenuation of early airway obstruction by mesenchymal stem cells in a murine model of heterotopic tracheal transplantation

Long-term success in lung transplantation is limited by obliterative bronchiolitis (OB). Presently, complete understanding of the mechanisms of OB has been elusive. Bone marrow-derived mesenchymal stem cells (MSC) have been shown to modulate repair of the injured lung in multiple disease models. We hypothesized that the injection of MSC would prevent development of early airway obstruction (AO) in the heterotopic tracheal transplant model. Forty-four tracheas from BALB/c and C57BL/6 donors were transplanted into 22 C57BL/6 recipients. At the time of transplant, 13 of the allogeneic recipient mice were injected with 5 × 10(5) MSC from various murine sources. To confirm the role of the immune response in the generation of AO we used a permeable inhibitor of nuclear factor-kappaB (NF-κB) in 11 recipients after transplantation with 22 BALB/c tracheas. After transplantation, administration of MSC inhibited intraluminal obstruction by collagen in 98% of the mice and transforming factor-beta (TGF-β) expression decreased to levels similar to those observed in isograft controls. These effects were associated with a significant (p < 0.05) increase in expression of the anti-inflammatory cytokine interleukin-10 (IL-10). NF-κB inhibitor showed decreased expression of transforming growth factor-beta (TGF-β) in the Day 7 and Day 14 groups, resulting in a 60% reduction of luminal obstruction as well as a decrease in inflammatory cells to the airway. Our observations suggest that administration of MSC prevents development of airway occlusion in a mouse model, probably through the modulated immune response altering TGF-β expression.

Dose-response Effects of Bleomycin on Inflammation and Pulmonary Fibrosis in Mice

Many studies have reported that bleomycin, anti-cancer drug, induces pulmonary fibrosis as a side effect. However, few investigations have focused on the dose-response effects of bleomycin on pulmonary fibrosis. Therefore, in the present study, we investigated the effects of different doses of bleomycin in male mice. ICR mice were given 3 consecutive doses of bleomycin: 1, 2, or 4 mg/kg in bleomycin-treated (BT) groups and saline only in vehicle control (VC) groups. The animals were sacrificed at 7 and 24 days postinstillation. The severity of pulmonary fibrosis was evaluated according to inflammatory cell count and lactate dehydrogenase (LDH) activity in the broncho alveolar lavage fluid (BALF) , and lung tissues were histologically evaluated after hematoxylin and eosin (H&E) , and Masson’s trichrome staining. BT groups exhibited changed cellular profiles in BAL fluid compared to the VC group, which had an increased number of total cells, neutrophils, and lymphocytes and a modest increase in the number of macrophages at 7 days post-bleomycin instillation. Moreover, BT groups showed a dose-dependent increase in LDH levels and inflammatory cell counts. However, at 24 days after treatment, collagen deposition, interstitial thickening, and granulomatous lesions were observed in the alveolar spaces in addition to a decrease in inflammatory cells. These results indicate that pulmonary fibrosis induced by 4 mg/kg bleomycin was more severe than that induced by 1 or 2 mg/kg. These data will be utilized in experimental animal models and as basic data to evaluate therapeutic candidates through non-invasive monitoring using the pulmonary fibrosis mouse model established in this study.

Effect of oral tolerance in a mouse model of allergic rhinitis

Objective Induction of oral tolerance (OT) is known to prevent allergic inflammation in models of asthma. This study investigated the preventive effect of OT and airway remodeling in a mouse model of allergic rhinitis (AR). Study Design An in vivo study using an animal model. Setting Catholic Research Institutes of Medical Science. Methods Forty six-week-old, female BALB/c mice were divided into four groups: control, AR, low-dose OT, and high-dose OT. To induce OT, mice were fed ovalbumin (OVA) before sensitization with OVA/aluminum hydroxide, 1 mg for six days in the low-dose OT group and a 25 mg single dose in the high-dose OT group. Mice in the AR group were fed phosphate-buffered saline. After sensitization followed by challenges with OVA during six weeks, nasal behaviors, interleukin (IL)-13 and interferon gamma (IFN-γ) levels in nasal lavage (NAL) fluids, as well as OVA-specific IgE levels in serum, were measured. The degree of goblet cell hyperplasia and thickness of lamina propria were observed in nasal tissues by periodic acid-Schiff and Masson's trichrome stain. A P value < 0.05 was accepted as statistically significant. Results Both OT groups showed a significant decrease in inflammatory cells, IL-13 and IFN-γ in NAL fluids, as well as OVA-specific IgE levels in serum compared with the AR group. In addition, the degree of goblet cell hyperplasia and thickness of lamina propria were attenuated in both OT groups compared with the AR group. Further, these alterations did not differ significantly between the two OT groups. Conclusion These results suggest that OT may effectively reduce allergic inflammation as well as airway remodeling in a mouse model of AR.

Signs of anin situinflammatory reaction in scars of human American tegumentary leishmaniasis

Skin inflammation plays an important role during the healing of American tegumentary leishmaniasis (ATL), the distribution of cells in active lesions may vary according to disease outcome and parasite antigens in ATL scars have already been shown. We evaluated by immunohistochemistry, 18 patients with 1- or 3-year-old scars and the corresponding active lesions and compared them with healthy skin. Small cell clusters in scars organized as in the active lesions spreaded over the fibrotic tissue were detected, as well as close to vessels and cutaneous glands, despite a reduction in the inflammatory process. Analysis of 1-year-old scar tissue showed reduction of NOS2, E-selectin, Ki67, Bcl-2 and Fas expression. However, similar percentages of lymphocytes and macrophages were detected when compared to active lesions. Only 3-year-old scars showed reduction of CD3(+), CD4(+) and CD8(+)T cells, in addition to reduced expression of NOS2, E-selectin, Ki67 and BCl-2. These results suggest that the pattern of cellularity of the inflammatory reaction observed in active lesions changes slowly even after clinical healing. Analysis of 3-year-old scars showed reduction of the inflammatory reaction as demonstrated by decrease in inflammatory cells and in the expression of cell-activity markers, suggesting that the host-parasite balance was only established after that period.

Ocular Burn: Rinsing and Healing with Ionic Marine Solutions and Vegetable Oils

Purpose: We investigated the effects of various rinsing and healing protocols on corneal wound repair and inflammation following alkali burn in rabbits. Methods: We conducted in vitro, in vivo and ex vivo studies. First, different rinse solutions were tested in vitro after incubation of ocular cells with methanol or NaOH. Cell viability was then assessed using the neutral red test (cytofluorometry). Second, NaOH was applied to rabbit corneas and associations of rinse solutions (NaCl 0.9% or controlled ionization marine solutions) with N-acetylcysteine or vegetable oils (from Calophyllum inophyllum and Aleurites moluccana) were tested in vivo. The regeneration of the corneal epithelium and the infiltration of inflammatory cells were evaluated using in vivo confocal microscopy and ex vivo histological cuts. Results: The association of a controlled ionization marine solution with 10% C. inophyllum oil and 90% A. moluccana oil induced regeneration of the corneal epithelium and a decrease in inflammatory cells. Conclusions: Irrigation with marine solution followed by treatment with a mixture of C. inophyllum and A. moluccana oils is a promising treatment for ocular burns.