The Impacts of Chrysanthemum indicum Extract on Oxidative Stress and Inflammatory Responses in Adjuvant-Induced Arthritic Rats

Abstract

Chrysanthemum indicum has been used as a therapeutic agent against inflammation, hypertension, and respiratory conditions for many years. This research's aim has been to examine the antioxidant impacts that Chrysanthemum indicum extract (CIE) has on the oxidative stress and inflammatory responses in adjuvant-induced arthritic (AA) rats. 40 rats were categorised into 4 groups according to a completely randomized approach: Group I involved normal control rats (CTRL) that received a basal diet; Group II involved arthritic control rats (CTRL-AA) that received the same diet; Group III involved rats that received a basal diet and 30 mg/kg CIE; and Group IV involved arthritic rats with the same diet as Group III rats (CIE-AA). After injection with complete Freund's adjuvant, body weight, arthritis score, and the serum levels of TNF-α, IL-1β, IL-6, myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) were assessed. The results demonstrated that CIE delayed the onset time of arthritis and decreased the clinical arthritis severity score (P < 0.05). Observations of CIE-AA and CTRL-AA rats demonstrated that CIE alleviates oxidative stress and inflammatory responses in CIE-AA group. In conclusion, CIE alleviated oxidative stress and inflammatory responses, thereby highlighting its potential use as a candidate for clinical treatments of rheumatoid arthritis.

Figure 1

Body weight gain and arthritis index scores for Groups I–IV. (a) Body weight gain on day 7 and day 14; (b) arthritis index score from day 0 to day 14 following adjuvant injection. Arthritis was found to lower body weight gain while IF-AA treatment facilitated a rise in body weight gain when considered in relation to the CTRL-AA group. Data are expressed as means ± SEM (n = 10). ^A,BDifferent from each other (P < 0.05).

Figure 2

The preventative impact of CIE on the level of (a) MPO, (b) MDA, (c) GSH-Px, and (d) SOD values for the AA model. Data indicated with different superscript letters were statistically dissimilar (P < 0.05; n = 10).

Figure 3

The preventative impact of CIE on the level of (a) TNF-α, (b) IL-1β, and (c) IL-6 values for the AA model. Data indicated with different superscript letters were statistically dissimilar (P < 0.05; n = 10).

Figure 4

The impact of CIE on NF-κB activation. NF-κb were evaluated by assessing p65 DNA binding in joint. Data indicated with different superscript letters were statistically dissimilar (P < 0.05; n = 10).