MATERIALS AND METHODS: In the present study, our objective was to explore the potential of Citrus aurantifolia peel extract (CAPE) on 2, 4, 6-trinitrobenzene sulfonic acid (TNBS) induced colitis in mice. Twenty-eight male Balb/c mice were divided into four groups: (1) normal group, (2) TNBS group, (3) 125 mg/kg CAPE group and (4) 250 mg/kg CAPE group. Colitis was induced through rectal administration of TNBS. The anti-inflammatory effects of CAPE against colitis were assessed by body weight, DAI score, colonic length, weight-to-length ratio, haematology profile and histopathological examinations.
RESULTS: Our results showed that CAPE maintained the body weight of mice, repressed the increase of DAI score, maintained mice colonic length and weight, improved blood profile and suppressed the excessive production of TNF-α, IL-6 and IL-1β. Furthermore, CAPE improved the histopathological score of colitis mice.
CONCLUSION: All the findings of this study suggested that Citrus aurantifolia peel extract may be a potential natural agent for protecting mice against TNBS-induced colitis.
METHODS: hrCRP was expressed in E. coli Rosetta-gami and extracted from the SDS-PAGE gel. Male BALB/c mice were inoculated subcutaneously at the base of their tails by 1 × 105 stationary-phase of Leishmania major promastigotes (MHRO/IR/75/ER) suspended in sterile phosphate buffered saline (PBS). Nodules and subsequently, ulcers developed 14 days post-injection. 1.5 µg of the purified protein was administered on lesions of pre-infected mice by Leishmania major in the intervention group for five consecutive days.
RESULTS: The mean area of the lesions was decreased by about seven folds in the intervention group as compared to the control group after two weeks of the treatment (p = 0.024). The results were verified by the real-time polymerase chain reaction so that the parasite burden was determined 27 times in the control group as compared to the intervention group (p = 0.02). Two weeks after treatment, the conversion of the lesions to scars in the intervention group was observed.
CONCLUSION: The results indicate a potential therapeutic role for hrCRP in improving cutaneous leishmaniasis due to Leishmania major in mice models. The healing was in a stage-dependent manner.
AIM: The objective of this study was to assess the impact of ethyl acetate extract of fungus comb (EAEFC) on the inflammatory reaction in the spleen of mice induced by intraperitoneal injection of lipopolysaccharide (LPS).
METHODS: An experimental study was conducted using a post-test-only control group design with male BALB/C mice (n = 24). The mice were divided randomly into four groups, each comprising six mice, and administered substances via gavage. Groups I and III were administered a solution of 5% dimethyl sulfoxide (DMSO) in distilled water, while Groups II and IV were given 500 mg/kg BW EAEFC dissolved in 5% DMSO. On the fifteenth day, Groups I and II received intraperitoneal injections of 5 ml/kg BW saline, while Groups III and IV were injected with 10 mg/kg BW LPS dissolved in saline. After three hours, the mice were euthanized and splenic immunohistology was examined under a light microscope. The results were expressed as mean ± standard deviation, while the group differences were assessed statistically.
RESULTS: The expression of interleukin (IL)-1, furin, and activated NK cell was significantly higher in the inflamed model after EAEFC supplementation, while the extract suppressed IL-10.
CONCLUSION: EAEFC was found to alter cytokine expression in the spleen in response to inflammation.
Materials and Methods: Twenty-five ICR mice and 20 BALB/C mice were used where five animals as control and the rest were randomly divided into four time points at 5, 10, 24 and 48 hours post-dosing (hpd). They were induced with 500 mg/kg APAP intraperitoneally. Liver sections were processed for hematoxylin-eosin staining and histopathological changes were scored based on grading methods.
Results: Intense centrilobular damage was observed as early as 5 hpd in BALB/C as compared to ICR mice, which was observed at 10 hpd. The difference of liver injury between ICR and BALB/C mice is due to dissimilarity in the genetic line-up that related to different elimination pathways of APAP toxicity. However, at 24 hpd, the damage was markedly subsided and liver regeneration had taken place for both ICR and BALB/C groups with evidence of mitotic figures. This study showed that normal liver architecture was restored after the clearance of toxic insult.
Conclusion: AILI was exhibited earlier in BALB/C than ICR mice but both underwent liver recovery at later time points.