Objective: This study was carried to investigate the role of chitosan nanoparticle in protecting against cadmium chloride-induced gastric toxicity in the rat. Methods: The 50 male rats were divided into 5 group: negative control (Rats were given daily with aquadest) ; positive control (Rats were given daily with cadmium chloride 5 mg/kg BW orally once in a day for 28 days) and the treatment group (Rats were given the chitosan nanoparticle 150 mg; 300 mg; 600 mg/kg BW orally once in a day for 32 days and on 4 th day, were given cadmium chloride 5 mg/kg BW one hour after the chitosan nanoparticle administration for 28 days). On day 32, the rats were sacrificed, and gastric tissues were collected to measure Malondialdehyde (MDA), Superoxide Dismutase (SOD), Glutathione Peroxidase (GPx) and histological evaluations. Results: Oral administration of cadmium chloride 5 mg/kg BW for 28 days significant induced gastric mucosal hemorrhagic lesions, increase MDA, decrease SOD and GPx, and also caused necrosis of gastric mucosal epithelial cell in the rat. Treatment with the chitosan nanoparticle 600 mg/kg BW but not 150 mg/kg BW and 300 mg/kg BW significantly improved gastric injury, decreased MDA, increase in SOD and GPx levels, and also improved necrosis of gastric mucosal epithelial cell as compared to positive control group. Conclusion: From the results of this study concluded that the chitosan nanoparticle could be a potent natural product provide a promising gastroprotective effect against cadmium chloride induced gastric toxicity in rats.This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.
Objective:It has long been known that chickens, like mammals, are capable of producing antigen-specific immunoglobulin Y (IgY), which functions similar to IgG. The present study was performed to investigate the activity of IgY anti-Mycobacterium tuberculosis on proliferation, interleukin (IL)-2, and interferon (IFN)-γ expression of rat peripheral blood mononuclear cells (PBMCs).Materials and Methods:The activity of IgY anti-M. tuberculosis in different doses (25, 50, and 100 μg/ml) on rat PBMCs proliferation was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay. The production of IL-2 and IFN-γ in the PBMC supernatant was determined using enzyme-linked immunosorbent assay. Investigation was performed on mRNA expression of IL-2 and IFN-γ by reverse transcription-polymerase chain reaction (RT-PCR).Results:IgY anti-M. tuberculosis significantly increased the proliferation of rat PBMC. Furthermore, IgY anti-M. tuberculosis dose dependently increased IL-2 and IFN-γ production in PBMC, suggesting that pharmacological activities of IgY anti-M. tuberculosis in PBMC may be mediated by regulating the production of cytokines. In the RT-PCR, expression of cytokines such as IL-2 and IFN-γ in PBMC cultures was increased by IgY anti-M. tuberculosis.Conclusions:We concluded that increasing IL-2 and IFN-γ productions in PBMC was related to IgY anti-M. tuberculosis, stimulating the mRNA transcription (gene expression) of these cytokines which can induce proliferation of PBMC.SUMMARY Lohman laying hens immunized intramuscularly with antigens of M. tuberculosis can produce specific IgY anti-Mycobacterium tuberculosis complexIgY anti-M. tuberculosis significantly increased the proliferation of rat peripheral blood mononuclear cell (PBMC)IgY anti-M. tuberculosis dose dependently increased interleukin 2 (IL-2) and interferon (IFN)-γ production in PBMCIn the reverse transcription-polymerase chain reaction, expression of cytokines such as IL-2 and IFN-γ in PBMC cultures was increased by IgY anti-M. tuberculosisThe increasing IL-2 and IFN-γ productions in PBMC were related to stimulation on mRNA transcription which can induce proliferation of PBMC. Abbreviations Used: IgY anti-M. tuberculosis: Immunoglobulin Y anti-Mycobacterium tuberculosis; IL-2: Interleukin-2; IFN-γ: Interferon-γ; PBMCs: Peripheral blood mononuclear cells.
The current study was carried out to evaluate the antioxidant and anti-caspase 3 activity of chitosan- Pinus merkusii nanoparticle in against lead acetate-induced nephrotoxicity in rats. chitosan- P. merkusii nanoparticle was characterized by dynamic light scattering (DLS) and scanning electron microscope (SEM). The male rats were divided into control group (rats were given with distilled water), lead acetate group (rats were injected with lead acetate 15 mg/kg BW i. p), and the treatment group (rats were given the chitosan- P. merkusii nanoparticle 150 mg, 300 mg, 600 mg/kg BW orally and were injected with lead acetate 15 mg/kg BW). The rats blood samples were measured levels of blood urea nitrogen (BUN) and creatinine. The kidney tissues were collected to evaluate the malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx). Histological to evaluate renal damage, and immunohistochemical to analyze the expression of caspase 3. The results showed that DLS showed the size of chitosan- P. merkusii nanoparticle was 165.9 ± 24.18 nm. SEM images of the chitosan- P. merkusii nanoparticles showed an irregular shape and its the rough surface. Administration of lead acetate resulted in a significant increase in levels of the BUN, creatinine, MDA level, caspase 3 expression, and a decrease in SOD and GPx were compared with the control group. Treatment with the chitosan- P. merkusii nanoparticle 600 mg/kg BW significantly decreased the elevated BUN, creatinine, MDA levels, caspase 3 expression and also increase in SOD and GPx as compared to lead acetate group. The lead acetate induced loss of the normal structure of renal cells and necrosis, whereas treated with chitosan- P. merkusii nanoparticle improved renal cell necrosis. This study indicates that chitosan- P. merkusii nanoparticles appeared to be a promising agent for protection against lead-induced nephrotoxicity through increasing antioxidant and inhibiting caspase 3 expression.
This study, we investigated the role of Chitosan-Pinus merkusii extracts nanoparticle in against lead acetate-induced cardiac cell damage in rat. Chitosan-Pinus merkusii extract nanoparticle was characterized by Scanning Electron Microscope (SEM) and Dynamic Light Scattering (DLS) .The fifty rats were divided into: control group (rats were given with distilled water); lead acetate group (rats were injected with lead acetate 15 mg/kg body weight i.p.), and the treatment group (rats were given the chitosan-Pinus merkusii nanoparticle 100mg; 200 mg; 400 mg/kg body weight orally and were injected with lead acetate 15 mg/kg BW). The blood was taken to be measured lactate dehydrogenase (LDH) and Creatinine Kinase-MB (CK-MB) level. Also the cardiac tissues were collected to evaluate the malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), and histological evaluations of heart damage. The size of Chitosan-Pinus merkusii extract nanoparticle in the DLS was 201.8±14.6 nm, while in the SEM showed an irregular shape and rough surface. The lead acetate significant increased LDH, CK-MB,MDA, and decreased SOD, GPx. Histological analysis, lead acetate also induced necrosis in the cardiac cell. However, treatment with the Chitosan-Pinus merkusii extract nanoparticle, only dose400 mg/kg BW significantly decreased LDH, CK-MB, MDA, and increased SOD, GPx levels. The Chitosan-Pinus merkusii extract nanoparticle 400 mg/kg BW also demonstrated significantly improved cardiac cell damage. From the results, it is concluded that the Chitosan-Pinus merkusii nanoparticle is a potent antioxidant in against lead acetate-induced cardiotoxicity in rats.
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