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<p>Osteoarthritis (OA) primarly involves the degradation of joint cartilage and requires new treatments. REJENERA<sup>©</sup>, a newly developed nutraceutical formula against OA, contains primarily olive leaf bioflavonoids ( ZeyEX<sup>©</sup>, quercetin and luteolin), <i>S</i>-allylcysteine, palmitoylethanolamide, <span>l</span>-proline, hyaluronic acid and boron. This study focuses on the efficacy of REJENERA in treating knee OA and aims to compare it with ZeyEX, NPROC<sup>©</sup> (a product obtained by combining collagen-rich eggshell membrane with olive leaf extract), and IBUPROFEN in a rat OA model. OA was established by intra-articular injection of monosodium iodoacetate (MIA; 3&#xa0;&#xa0;mg) into the right knee joints. Rats were either left untreated or treated orally for 12&#xa0;weeks with REJENERA, ZeyEX, NPROC (300&#xa0;mg/kg/day) or IBUPROFEN (3&#xa0;mg/kg/day). MIA injection produced joint degeneration including increased fissure-index, osteophyte-score, and OARSI-score, joint swelling, synovial inflammation, proteoglycan loss, and decreased cartilage thickness. These histopathological abnormalities were partially but significantly alleviated by REJENERA and other treatments. Only ZeyEX significantly inhibited the OA-induced increase in IL-1β, IL-6, IL-10 and LPO in serum, and IL-6, TNF-α, and IFN-γ in synovial fluid. While increases in MMP-3 and MMP-9 were reduced with all treatments, MMP-13 was inhibited only by REJENERA. ZeyEX increased IL-2, NPROC increased IL-6, and IBUPROFEN inhibited IL-10. All treatments improved TIMP-1 levels; however, TXNIP was more significantly inhibited by ZeyEX, and NLRP3 by REJENERA. REJENERA’s anti-OA effects are accompanied by an increase in cartilage anabolic factors (Ki-67, type-II collagen, BMP-7) and inhibition of apoptosis. REJENERA offers a promising multi-targeted therapeutic approach to treating OA by blocking the iNOS-TXNIP-NLRP3&#xa0;signaling axis, and reducing oxidative stress.</p>

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REJENERA©, a multi-component bioflavonoid-based formula, alleviates osteoarthritis and provides chondroprotection by regulating the NLRP3-TXNIP-iNOS axis and inflammation: a comparative study with olive leaf nutraceuticals and ibuprofen

  • 期刊论文

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  • 发表日期：

    2026年7月6日

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  • Huseyin Emre Tepedelenlioglu,
  • Zubeyir Elmazoglu,
  • Sanem Gulistan Saribas,
  • Yildiz Tutuncu,
  • Asli F. Ceylan,
  • Çimen Karasu

摘要

Osteoarthritis (OA) primarly involves the degradation of joint cartilage and requires new treatments. REJENERA©, a newly developed nutraceutical formula against OA, contains primarily olive leaf bioflavonoids ( ZeyEX©, quercetin and luteolin), S-allylcysteine, palmitoylethanolamide, l-proline, hyaluronic acid and boron. This study focuses on the efficacy of REJENERA in treating knee OA and aims to compare it with ZeyEX, NPROC© (a product obtained by combining collagen-rich eggshell membrane with olive leaf extract), and IBUPROFEN in a rat OA model. OA was established by intra-articular injection of monosodium iodoacetate (MIA; 3  mg) into the right knee joints. Rats were either left untreated or treated orally for 12 weeks with REJENERA, ZeyEX, NPROC (300 mg/kg/day) or IBUPROFEN (3 mg/kg/day). MIA injection produced joint degeneration including increased fissure-index, osteophyte-score, and OARSI-score, joint swelling, synovial inflammation, proteoglycan loss, and decreased cartilage thickness. These histopathological abnormalities were partially but significantly alleviated by REJENERA and other treatments. Only ZeyEX significantly inhibited the OA-induced increase in IL-1β, IL-6, IL-10 and LPO in serum, and IL-6, TNF-α, and IFN-γ in synovial fluid. While increases in MMP-3 and MMP-9 were reduced with all treatments, MMP-13 was inhibited only by REJENERA. ZeyEX increased IL-2, NPROC increased IL-6, and IBUPROFEN inhibited IL-10. All treatments improved TIMP-1 levels; however, TXNIP was more significantly inhibited by ZeyEX, and NLRP3 by REJENERA. REJENERA’s anti-OA effects are accompanied by an increase in cartilage anabolic factors (Ki-67, type-II collagen, BMP-7) and inhibition of apoptosis. REJENERA offers a promising multi-targeted therapeutic approach to treating OA by blocking the iNOS-TXNIP-NLRP3 signaling axis, and reducing oxidative stress.