Aim. This study is aimed at evaluating the use of curcumin-loaded polylactic-co-glycolic acid nanoparticles (CUR-loaded PLGA NPs) as a treatment against monosodium iodoacetate- (MIA-) induced knee OA. Materials and Methods. Eighteen rats were assigned to three groups ( ), namely, normal control group that received intra-articular injections (IAIs) of saline, an OA control group that received an IAIs of MIA (2 mg/50 μL), and a treatment group (MIA+CUR-loaded PLGA NPs) that received IAIs of CUR-loaded PLGA NPs (200 mg/kg b.wt). Results. The CUR NP treatment against knee OA alleviated radiographic alternations and histopathological changes and inhibited the upregulation in the serum levels of interleukin-1β, tumor necrosis factor-α, interleukin-6, and transforming growth factor-beta and the downregulation in interleukin-10. CUR NP-treated joints also decreased the mRNA expression of nuclear factor-kappa B and inducible nitric oxide synthase and the protein expression of matrix metalloproteinase-13 and caspase-3. Finally, CUR-loaded PLGA NP treatment mitigated the loss of type II collagen, which resulted in a significant reduction in malondialdehyde level and increased the glutathione content and superoxide dismutase activity compared with that of the OA group. Conclusion. This study demonstrated that the administration of CUR NPs could provide effective protection against MIA-induced OA and knee joint histological deteriorated changes due to its anti-inflammatory, antioxidant, and antiapoptotic properties.

Osteoarthritis (OA) of the knee is a debilitating condition that can severely limit an individual’s mobility and quality of life. This study was designed to evaluate the efficacy of bone marrow-derived mesenchymal stem cell (BM-MSC) treatment in cartilage repair using a rat model of monoiodoacetate- (MIA-) induced knee OA. OA was induced in the knee joint of rats by an intracapsular injection of MIA (2 mg/50 μL) on day zero. The rats were divided into three groups ( ): a normal control group, an osteoarthritic control group, and an osteoarthritic group receiving a single intra-articular injection of BM-MSCs ( cells/rat). The knee diameter was recorded once per week. By the end of the performed experiment, X-ray imaging and enzyme-linked immunosorbent assay analysis of serum inflammatory cytokines interleukin-1beta (IL-β), IL-6, and tumor necrosis factor-α (TNF-α) and anti-inflammatory cytokines interleukin-10 and transforming growth factor-beta (TGF-β) were carried out. In addition, RT-PCR was used to measure nuclear factor-kappa B (NF-κB), inducible nitric oxide synthase (iNOS), and type II collagen mRNA levels and Western blot analysis was used to determine caspase-3 protein levels in all treated groups. Finally, hematoxylin/and eosin stains were used for histopathological investigation. Administration of BM-MSCs significantly downregulated knee joint swelling and MIA-induced (IL-1β, IL-6, and TNF-α) and upregulated IL-10 and TGF-β as well. Moreover, BM-MSC-treated osteoarthritic rats exhibited decreased expression of NF-κB, iNOS, and apoptotic mediator (caspase-3) and increased expression of type II collagen when compared to rats treated with MIA alone. The hematoxylin/eosin-stained sections revealed that BM-MSC administration ameliorated the knee joint alterations in MIA-injected rats. BM-MSCs could be an effective treatment for inflamed knee joints in the MIA-treated rat model of osteoarthritis, and the effect may be mediated via its anti-inflammatory and antioxidant potential.

The safety of using monosodium glutamate (MSG) as a food flavour enhancer has generated much controversy locally and globally. Quercetin (QU), a natural compound of multiple origins, has broad biopharmacological effects as an antioxidant and a hepatoprotective substance. Therefore, the present study was designed to investigate the modulatory effect of oral doses of QU on the microscopic liver changes and liver oxidative stress induced by MSG. Thirty male albino rats were divided into five groups, each of six rats: group I received distilled water, group II received corn oil, group III was administered QU (14 mg/kg body weight), group IV was treated with aqueous MSG (15 mg/kg body weight), and group V was given MSG (15 mg/kg body weight) simultaneously with QU (14 mg/kg body weight), orally and daily for 30 days. Numerous deleterious histological and ultrastructural changes were induced by MSG in concomitant with a significant increase in the activities of serum aminotransferases (ALT and AST) and the level of hepatic lipid peroxidation, while decreases in superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, as well as reduced glutathione (GSH) concentration were also recorded. QU administration amended the liver histological lesions and ultrastructural changes induced by MSG via decreasing significantly the level of hepatic lipid peroxidation and the leakage of serum aminotransferases, and improving the hepatic antioxidant defence system. In conclusion, QU showed a hepatoprotective activity against the potential toxicity of MSG food flavour.