This study aims to evaluate the anti-inflammatory effect of Auricularia auricula-judae ethanol extract (AEE) in LPS-induced RAW264.7 cells and dextran sulfate sodium (DSS)-induced acute colitis mice. The highest levels of total polyphenols and DPPH radical scavenging activity were observed in AEE. Also, NO production was reduced in a dose-dependent manner in RAW264.7 cells stimulated by lipopolysaccharide (LPS). AEE was suspended in distilled water and administration per oral at different doses of 100 and 300 mg/kg body weight every day with 3% DSS in drinking water for 7 days. The sample AEE 100 and 300 mg/kg significantly increased body weight, colon length and decreased disease activity index (DAI) score. Histological features showed that 100 and 300 mg/kg of AEE suppressed edema, mucosal damage and the loss of crypts induced by DSS. The serum levels of TNF- and IL-6 were measured in acute colitis mice using ELISA kits. Levels of TNF- and IL-6 in serum were significantly decreased by topical application of AEE. Therefore, AEE increases antioxidant and anti-inflammatory activity, and it is thought that it can effectively help prevent colitis.
This study observed the anti-inflammatory effect of the polysaccharide derived from the mycelium of Tremella fuciformis in mice with colitis induced with dextran sulfate sodium (DSS). The experimental groups were normal, DSS, DSS-TFL50, DSS-TFH100, and suflasalazine. Body weights, colon lengths, and organ weights were measured, and the plasma level of pro-inflammatory cytokine and mRNA and protein expression in colon tissue were analyzed. Body weight loss, a symptom of DSS-induced colitis, was suppressed by DSS-TF and the speed of weight recovery proceeded rapidly. In addition, DSS-TF showed a significant inhibitory effect on the decrease of colon length typically caused by colon damage. TNF-α, IL-6 and IL-1β cytokine levels in plasma were reduced in DSS-TF and positive control groups. TNF-α, COX-2 and IL-1β mRNA expression in colon tissue were inhibited in DSS-TF and positive control, and it was significantly different from that of the DSS group. The protein expression of inflammation-related genes (IL-6, TNF-α and COX-2) in the colon tissue was significantly increased by DSS compared to that of the normal group, but by DSS-TFL50, DSS-TFH100 and sulfasalarin decreased. In conclusion, the polysaccharide derived from the mycelium of Tremella fuciformis showed the anti-inflammatory effect on DSS-induced colitis in mice.
L. brevis HY7401, L. helveticus HY7801 및 B. longum HY8004의 복합유산균 R&B Balance®의 대장염 개선 효과를 DSS 처리 마우스에서 평가하였다. R&B Balance® 섭취에 의해 대장길이 축소, MPO 활성과 같은 대장염 증상이 감소하였으며, 분변내 chondrointinase 활성과 분변 유전독성을 현저하게 감소시키는 것으로 나타났다. T-RFLP pattern의 군집 분석 결과, DSS-유도 대장염 마우스의 미생물총은 정상적인 마우스와 다르며, R&B Balance®의 투여는 장내 미생물총의 다양성에 영향을 미칠 수 있음을 확인하였다. 따라서 R&B Balance®는 DSS로 유도된 대장염 동물에서 대장염 증상을 개선해주고 분변 내 독성 효소나 유독한 대사산물을 생성을 억제함으로써 대장염을 개선하는 것으로 판단되고 대장염 동물의 장내 미생물 다양성에도 영향을 미치는 것으로 확인되었다.
This study was conducted to investigate the anti-inflammatory effects of Pruns mume, Schisandra chinensis, Chaenomeles sinensis-- Prunus mume mixtrue (PM) treatment on colitis induced in mice by dextran sodium sulfate (DSS) treatment. A total of 25 male BALB/c mice (average weight 20.7 ± 1.6 g) were divided into 5 treatment groups and fed a commercial diet (A), PM administration (B), commercial diet + induced colitis by DSS (C), PM administration + induced colitis by DSS (D) and sulfasalazine + induced colitis by DSS (E). We found that PM treatment (D) and sulfasalazine (E) decreased the expression of TNF-α and COX-2 compared to the DSS-induced colitis group (C). The expression of IL-4, STAT6, IFN-γ, STAT1 was decreased in group D and group E compared to the colitis group (C), COX-2 and STAT1 were more decreased in group D. The serum IgE levels decreased in the PM treatment groups (C and D) compared to the non-PM treatment groups (A and B) although there was no significant difference between the PM treatment groups. It is notable that a therapeutic application of the PM extracts ameliorated DSS-induced colitis in mice.