Abstract
The present work aimed to assess the chondroprotective influence of chitosan and lecithin in a monoiodoacetate (MIA)-induced experimental osteoarthritis (OA) model. Forty male rats weighing 180–200 g were randomly distributed among the following five experimental groups (eight per group): control, MIA-induced OA, MIA-induced OA + chitosan, MIA-induced OA + lecithin, and MIA-induced OA + chitosan + lecithin. The levels of TNF-α, IL6, RF, ROS, and CRP, as well as mitochondrial markers such as mitochondrial swelling, cytochrome C oxidase (complex IV), MMP, and serum oxidative/antioxidant status (MDA level) (MPO and XO activities) were elevated in MIA-induced OA. Also, SDH (complex II) activity in addition to the levels of ATP, glutathione (GSH), and thiol was markedly diminished in the MIA-induced OA group compared to in control rats. These findings show that mitochondrial function is associated with OA pathophysiology and suggest that chitosan and lecithin could be promising potential ameliorative agents in OA animal models. Lecithin was more effective than chitosan in ameliorating all of the abovementioned parameters.
Highlights
Osteoarthritis (OA) is a severe debilitating and painful condition characterized by the gradual reduction of the articular cartilages, joints’ swelling, and bone cysts [1]
The current results suggested that chitosan and lecithin administered in combination remarkably reduced the MMP collapse in OA group
The current study aimed to identify whether chitosan and/or lecithin improved the degeneration of the articular cartilage on OA-treated rats (Figure 9)
Summary
Osteoarthritis (OA) is a severe debilitating and painful condition characterized by the gradual reduction of the articular cartilages, joints’ swelling, and bone cysts [1]. During OA progress, a lot of inflammatory cytokines and prostaglandin E2 , are increased in the joint bodies of OA patients and animals with OA-like diseases [4]. Inflammatory reactions such as aging along with other treatment interactions, have been demonstrated to afford oxidative injury by excessive production and triggering of H2 O2. In this study, the effects of chitosan and lecithin on OA symptoms that were induced by monoiodoacetate (MIA) were investigated in details at the level of mitochondrial dysfunction, oxidative injury and TEM sections
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