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. 2020 Dec 4;25(23):5738.
doi: 10.3390/molecules25235738.

Chitosan and Lecithin Ameliorate Osteoarthritis Symptoms Induced by Monoiodoacetate in a Rat Model

Reham Z Hamza  1   2 , Fawziah A Al-Salmi  1 , Nahla S El-Shenawy  3
Affiliations

Chitosan and Lecithin Ameliorate Osteoarthritis Symptoms Induced by Monoiodoacetate in a Rat Model

Reham Z Hamza et al. Molecules. .

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.

Keywords: chitosan; lecithin; mitochondria; osteoarthritis; pathophysiology; rats.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Experimental protocol.
Figure 2
Figure 2
The efficacy of chitosan and lecithin against tumor necrosis factor-alpha (TNF-α) in (OA) model induced by monoiodoacetate (MIA). The data presented as mean ± S. E.
Figure 3
Figure 3
The efficacy of chitosan and lecithin against interleukin-6 (IL-6) in (OA) model that was induced by monoiodoacetate (MIA). The data presented as mean ± S. E.
Figure 4
Figure 4
The efficacy of chitosan and lecithin against: (A) C-reactive protein (CRP) and (B) rheumatoid factor (RF) of (OA) model that was induced by monoiodoacetate (MIA). The data presented as mean ± S. E.
Figure 4
Figure 4
The efficacy of chitosan and lecithin against: (A) C-reactive protein (CRP) and (B) rheumatoid factor (RF) of (OA) model that was induced by monoiodoacetate (MIA). The data presented as mean ± S. E.
Figure 5
Figure 5
The efficacy of chitosan and lecithin against: (A) succinate dehydrogenase (SDH) and (B) reactive oxygen species (ROS) in (OA) model induced by monoiodoacetate (MIA) in male rats. Where Fluorescence intensity (Relative wave length and content for DCF) (Indication for ROS content). The data presented as mean ± S. E.
Figure 6
Figure 6
The efficacy of chitosan and lecithin against mitochondrial membrane potential (MMP) in (OA) model induced by monoiodoacetate (MIA) in male rats. The data presented as mean ± S. E.
Figure 7
Figure 7
The efficacy of chitosan and lecithin against: (A) release of Cytochrome-C and (B) the mitochondrial swelling in (OA) model induced by monoiodoacetate (MIA) in male rats. The data presented as mean ± S. E.
Figure 7
Figure 7
The efficacy of chitosan and lecithin against: (A) release of Cytochrome-C and (B) the mitochondrial swelling in (OA) model induced by monoiodoacetate (MIA) in male rats. The data presented as mean ± S. E.
Figure 8
Figure 8
The efficacy of chitosan and lecithin against ATP contents in the (OA) model induced by monoiodoacetate (MIA) in male rats. The data given as mean ± S. E.
Figure 9
Figure 9
TEM section of the changes in the articular cartilage of the knee joints post-treatment with either chitosan and/or lecithin or combined after OA induction. Images showing collagen fibers of the following treated groups. (A) Control group: showing intact cartilage fibers (Orange arrow) with appearance of intact articular septa and intact chondrocyte (Green arrow) (Scale bar = 5 µm). (B) OA group (+ ve control group): showing atrophy of cartilage fibers (Inverted white arrows) with severe distortion of the articular septa (Whitehead arrow) and reduction in chondrocytes (Green arrow) (Scale bar = 5 µm). (C) OA group + Chitosan: showing some reduced chondrocyte (Green arrow) with most intact cartilage fibrils with the irregular articular septum (Inverted white arrow). (Scale bar = 5 µm). (D) OA group + Lecithin: showing moderate chondrocyte size (Red arrow) with intact cartilage fibrils (Inverted white arrow) and mild wide articular septum (Scale bar = 2 µm). (E) OA group + Chitosan +Lecithin: showing mostly high restoration of cartilage fibrils (Blue arrow) with mostly normal chondrocytes’ size (Green arrow) with appearance of intact and compact cartilage fibers and high restoration of the intra-articular septum (Scale bar = 2 µm). Table 2 clarifies the morphometric changes in all the treated groups and the rate of change in each treated group.
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