Platelet-Rich Plasma Combined with Alendronate Reduces Pain and Inflammation in Induced Osteoarthritis in Rats by Inhibiting the Nuclear Factor-Kappa B Signaling Pathway

Abstract

Purpose

Osteoarthritis (OA) is one of the common degenerative diseases of the joint in the world. This study was designed to explore the effect of platelet-rich plasma (PRP) combined with alendronate (ALN) on OA.

Methods

We induced OA model by anterior cruciate ligament transection (ACLT) method in rats and treating chondrocytes by IL-1 β in vitro. PRP and/or ALN were used to treat induced rats and chondrocytes. Hematoxylin and eosin (H&E) and Safranin O staining were used to observe the structures of cartilage. The mRNA expression of Collagen II, MMP-13, and inflammatory factors (IL-18, IL-1 β, and TNF- α) in the cartilage and chondrocytes of rats was determined by qRT-PCR. The expression of NF- κB pathway-related proteins (p-p65, p65, I κB α, and p-I κB α) in the cartilage and chondrocytes of rats was determined by Western blot. The proliferation of chondrocytes was detected by MTT assay.

Results

Treatment with PRP, ALN, or PRP combined with ALN decreased the degree of cartilage destruction, the mRNA expression of MMP-13 and inflammatory factors (IL-18, IL-1 β, and TNF- α), and the protein expression of p-I κB α/I κB α and p-p65/p65, increased Collagen II expression, and the threshold of tender and thermal pain in OA rats. Meanwhile, ALN, PRP, or ALN combined with PRP reversed the inhibiting effect of phorbol myristate acetate (PMA, an NF- κB agonist) on cell proliferation and cartilage matrix metabolism. Among them, the effects of ALN combined with PRP were most obvious.

Conclusion

PRP combined with ALN delayed OA progression by inhibiting the NF- κB signaling pathway.