Remember me
With the accelerating global population aging, the incidence of degenerative musculoskeletal diseases (such as osteoarthritis, osteoporosis, intervertebral disc degeneration and sarcopenia) continues to rise, posing a significant public health challenge. Current conventional therapeutic approaches, while alleviating symptoms, are often accompanied by side effects and struggle to reverse the pathological process. Garlic and its various active metabolites (such as allicin, S-allylmercaptocysteine, diallyl sulfide and diallyl disulfide, etc.) have been confirmed to possess multiple biological activities, including anti-inflammatory, antioxidant effects, regulation of signaling pathways, and maintenance of extracellular matrix homeostasis. Numerous studies have demonstrated that the active metabolites of garlic can intervene in degenerative musculoskeletal diseases by regulating multiple signaling pathways such as PI3K/Akt/NF-κB, RANKL/RANK/OPG, Wnt/β-catenin, and Akt/mTOR, significantly delaying the progression of the diseases. Therefore, this review summarizes the regulatory effects and potential mechanisms of garlic and its bioactive metabolites on degenerative musculoskeletal diseases, aiming to provide a scientific basis for the further development of adjunctive therapeutic strategies based on garlic active metabolites.
1 IntroductionDegenerative musculoskeletal diseases refer to a category of diseases characterized by chronic progressive degeneration or deterioration of the bones, cartilage, joints, and surrounding tissues (Wen et al., 2023). These conditions primarily encompass osteoarthritis, osteoporosis, intervertebral disc degeneration, and sarcopenia (Wen et al., 2023). Their clinical manifestations are predominantly characterized by progressively worsening pain, restricted mobility, and functional decline, accompanied by structural degenerative changes such as cartilage deterioration, reduced bone mineral density, and loss of muscle mass. In severe instances, these conditions can cause disabilities, greatly impacting patients’ quality of life and physical health. These diseases predominantly affect middle-aged and elderly populations and are a major factor contributing to functional impairment and reduced quality of life in older adults. The global aging process has led to a yearly rise in these disorders, increasing healthcare resource use and imposing significant socioeconomic burdens, thus representing a major global public health issue (Li and Chen, 2019). Current conventional treatment methods can alleviate symptoms to a certain extent, but they demonstrate limited efficacy in reversing pathological progression and are associated with issues such as drug dependence, disease recurrence, and surgical risks. Recent studies have indicated that natural metabolites found in onions, garlic, and tomatoes possess potential therapeutic effects against osteoarthritis (Salem et al., 2023), (Yang J. et al., 2020), with fewer side effects and a higher safety profile compared to traditional drugs. Consequently, exploring and developing novel, safe, and effective treatment strategies based on natural products, and delving into their regulatory mechanisms, holds significant scientific and clinical importance.
Garlic is a widely used aromatic herbaceous plant, valued both as a culinary ingredient and as a complementary treatment for various diseases (El-Saber Batiha et al., 2020). Garlic extracts and bioactive metabolites, rich in organosulfur compounds, polyphenols, flavanols, flavonoids, saponins, and tannins, exhibit therapeutic potential in orthopedic, cardiovascular, and metabolic diseases. They demonstrate multiple biological activities, such as analgesic, antithrombotic, antioxidant, anti-inflammatory, and antitumor effects (Tesfaye, 2021), (Huang et al., 2023), (Trio et al., 2014), (Pandey et al., 2023). Garlic’s main bioactive metabolites, organosulfur compounds, are divided into lipid-soluble types such as allicin, diallyl sulfide (DAS), diallyl disulfide (DADS), and diallyl trisulfide (DATS), and water-soluble types such as S-allyl cysteine (SAC) and S-allyl mercaptocysteine (SAMC) (Thomson and Ali, 2003) (Figure 1). Among these, allicin is a key bioactive substance. Upon enzymatic hydrolysis by alliinase, alliin is converted to allicin, which subsequently serves as a precursor for the generation of numerous bioactive derivatives, including DAS, DATS, and DADS (Sarvizadeh et al., 2021). Garlic and its bioactive metabolites exhibit multifaceted regulatory potential in degenerative musculoskeletal diseases. DAS has been shown to safeguard damaged chondrocytes by suppressing nuclear factor kappa-B (NF-κB) activation (Lee et al., 2009). Allicin mitigates IL-1β-induced inflammation in chondrocytes, reduces cartilage matrix degradation, and preserves cartilage tissue, thus slowing osteoarthritis progression (Qian et al., 2018). Clinical surveys indicate that garlic extract could be an adjunctive therapy for osteoarthritis (Zochling et al., 2004), (Dehghani et al., 2018), (Salimzadeh et al., 2018), emphasizing its potential value in treating degenerative musculoskeletal diseases. Accordingly, this review summarizes the regulatory effects of garlic and its bioactive metabolites, including their anti-inflammatory, antioxidant, and multi-signaling pathway modulatory activities, aiming to offer innovative research directions for natural product-based therapeutic strategies against degenerative musculoskeletal diseases (Table 1).
The classification and effects of active metabolites of garlic.
DiseasesGarlic derivativesMechanismsPublication dateReferencesOsteoarthritis (OA)Garlic Extract——2004Zochling et al. (2004)DASinhibit NF-κB pathwayGarlic and garlic derivatives and degenerative musculoskeletal diseases. ↓: downregulation, ↑: upregulation.
2 Literature search strategyThis narrative review aimed to provide a comprehensive overview of the current understanding of “The Impact of Garlic and Its Active Metabolites on Degenerative Musculoskeletal Diseases” comprehensively. Relevant studies were identified by searching the PubMed database. Keywords applied in the retrieval process included “Garlic”, “Allicin”, “Osteoarthritis”, “Osteoporosis”, “Intervertebral Disc Degeneration”, and their related synonyms. The search was primarily focused on articles published between 2004 and 2025, an emphasis on original research articles and clinical reports in the field. The inclusion of studies was based on their relevance to the core themes of this review, prioritizing original research and authoritative consensus statements. Given the considerable heterogeneity and methodological diversity of the existing literature on this subject, conditions for quantitative synthesis are not yet met. Therefore, a narrative review approach was adopted to integrate theoretical developments and research findings from a more comprehensive perspective. As a result, this review did not follow the PRISMA guidelines or other formal systematic review protocols.
3 The impact of garlic and its active metabolites on osteoarthritis regulationOsteoarthritis (OA) is a degenerative joint disease characterized by the progressive deterioration of articular cartilage. The primary clinical symptoms are pain, swelling, and joint stiffness, significantly hindering patient mobility. The pathological characteristics of OA encompass degradation of articular cartilage, changes in subchondral bone, and inflammation of the synovium (Samuels et al., 2008). OA development is influenced by various risk factors such as joint injury history, overuse, aging, and being overweight, with a higher incidence observed in women compared to men. The pathological mechanism of OA focuses on degenerative changes in articular cartilage, involving interconnected processes like inflammatory cytokine activation, extracellular matrix (ECM) metabolic imbalance in chondrocytes, dysregulated cellular signaling pathways, and oxidative stress. These factors collectively promote OA progression and establish a vicious cycle, ultimately resulting in joint structural destruction. Current OA treatment typically involves using nonsteroidal anti-inflammatory drugs and COX-2 selective inhibitors to reduce inflammation by blocking prostaglandin E2 synthesis. These agents are associated with toxicity and heightened risks of gastrointestinal bleeding (Park et al., 2006) and cardiovascular events. Consequently, natural metabolites are gaining attention for their potential therapeutic benefits and enhanced safety.
3.1 The regulatory effects of allicin on osteoarthritisInflammation is pivotal in OA progression, marked by increased pro-inflammatory cytokines like interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) (Park et al., 2006), (Ansari et al., 2020), (Kapoor et al., 2011), (Keller et al., 2023). These cytokines trigger the expression of matrix metalloproteinases (MMPs), inflammatory mediators, and reactive oxygen species (ROS), resulting in ECM degradation and joint dysfunction. Allicin treatment notably inhibits the PI3K/Akt/NF-κB signaling pathway activation induced by IL-1β in chondrocytes, a key mechanism in its action against OA (Qian et al., 2018). Furthermore, in a mouse model of surgically induced osteoarthritis, allicin treatment significantly reduced cartilage destruction, demonstrated by lower Osteoarthritis Research Society International scores (Qian et al., 2018). In vitro studies show that allicin inhibits IL-1β-induced overexpression of inflammatory mediators like nitric oxide (NO), prostaglandin E2, TNF-α, and IL-6, along with enzymes such as inducible nitric oxide synthase (iNOS) and COX-2, in a dose-dependent manner, thus reducing inflammation and ECM degradation (Qian et al., 2018). This effect is achieved by reducing NF-κB p65 nuclear translocation and IκBα degradation, thereby blocking downstream pro-inflammatory gene transcription. Chondrocytes in mature cartilage possess the capacity to proliferate and repair damaged cartilage tissue. In vitro experiments demonstrated that a 36-h allicin treatment significantly decreased the proportion of chondrocytes in the G0/G1 phase and increased those in the S-phase, accompanied by a notable upregulation of cyclin D1, CDK4, and CDK6 protein and mRNA expression. These findings indicate that allicin enhances chondrocyte proliferation and aids in cartilage tissue repair (Li et al., 2015). Furthermore, allicin reverses the IL-1β-induced overexpression of MMP-13 and restores the synthesis of type II collagen (Col II) and aggrecan, thereby maintaining the integrity of cartilage structure (Qian et al., 2018). Allicin not only possesses anti-inflammatory properties but also provides protection via antioxidant pathways. Oxidative stress, a key pathological mechanism in OA, is marked by an imbalance between elevated ROS production and reduced antioxidant capacity (Ansari et al., 2020). Nuclear factor erythroid 2-related factor 2 (Nrf2) is a crucial antioxidant transcription factor vital for cartilage integrity, with its dysfunction causing redox imbalance (Hecker et al., 2014). Under normal physiological conditions, Nrf2 is inactivated by binding to its negative regulator, Keap1. Research indicates that allicin mitigates H2O2-induced oxidative stress, decreases inflammatory factor expression, promotes cartilage matrix synthesis, and prevents chondrocyte hypertrophic differentiation through the activation of the Keap1/Nrf2 pathway, thus slowing OA progression (Yang J. et al., 2020).
3.2 The regulatory effects of SAMC on osteoarthritisDuring OA progression, the majority of cartilage undergoes progressive attrition over time, accompanied by an imbalance in the MMPs/TIMP-1 ratio, which leads to exacerbated degradation of Col II, a major component of the ECM. SAMC, a key water-soluble garlic derivative, exhibits antioxidant, anti-inflammatory, and antitumor properties (Zhu et al., 2017), (Li et al., 2017). SAMC dose-dependently suppresses MMP-9 and MMP-13 expression while upregulating TIMP-1, thereby restoring MMPs/TIMP-1 balance and attenuating Col II degradation (Yang et al., 2017). The SAMC-induced elevation in Col II protein expression, along with the reduction in its proteolytic product C2C, helps preserve cartilage structure integrity by indicating less articular cartilage destruction. Furthermore, SAMC treatment significantly elevates cytoplasmic IκBα levels and reduces nuclear p65 content, suggesting that it may exert anti-inflammatory effects through suppression of NF-κB pathway activation and downstream inflammatory signal transduction (Yang et al., 2017). Recent studies suggest that SAMC may have therapeutic potential in OA by influencing Nrf2 via the NOX4/NF-κB pathway modulation (Yang G. et al., 2020). In vitro experiments showed that SAMC improves the viability and proliferation of chondrocytes diminished by IL-1β stimulation. However, under unstimulated basal conditions, SAMC did not exhibit a proliferative effect on chondrocytes (Yang et al., 2017). Similarly, in surgically induced rat OA models and in IL-1β-stimulated chondrocytes, NADPH oxidase 4 (NOX4) was activated while the expression of Nrf2 and its negative regulator Keap1 decreased. Both low-dose (2 mM) and high-dose (5 mM) SAMC reversed this trend and alleviated inflammation, with the protective effect being particularly pronounced in the SAMC (5 mM) group. However, SAMC (5 mM) did not further activate Nrf2, and the specific mechanism underlying this observation requires further elucidation. SAMC enhances the expression of Nrf2-dependent antioxidant enzymes, mitigating ROS-induced cartilage collagen degradation and thereby alleviating OA. In Nrf2-knockout chondrocytes, SAMC treatment not only failed to reverse oxidative stress but instead further activated NOX4 expression, leading to an increased MMPs/TIMP-1 ratio and exacerbated Col II degradation. Furthermore, the inhibitory effects of SAMC on COX-2 and iNOS expression were abolished upon Nrf2 deletion (Yang G. et al., 2020). These findings indicate that the protective effects of SAMC on OA cartilage are partially dependent on Nrf2, with the mechanism potentially involving targeted regulation of Nrf2 through the NOX4/NF-κB signaling pathway.
3.3 The regulatory effects of DAS and DADS on osteoarthritisUnder inflammatory stimulation, the expression of COX-2 is upregulated in chondrocytes and synovial cells of human articular tissues (Lee et al., 2009), therefore, COX-2 overexpression in articular tissues represents a significant pathological feature of inflammatory arthropathies. In rat OA models and in vitro cellular experiments, DAS has been shown to significantly inhibit COX-2 expression induced by IL-1β or monosodium urate crystals in chondrocytes and synoviocytes. Inhibiting the NF-κB signaling pathway may mediate this effect, educing synovial inflammation and cartilage degradation, indicating DAS’s potential therapeutic value in OA treatment (Lee et al., 2009). Results from relevant in vitro studies have shown that DADS dose-dependently inhibits IL-1-induced expression of MMPs, such as MMP-1 and MMP-13, demonstrating its therapeutic potential to alleviate inflammation associated with OA (Williams et al., 2010). This study also indicated that DAS, in a manner similar to DADS, dose-dependently suppresses the expression of the aforementioned MMPs (Williams et al., 2010).
In summary, garlic and its bioactive metabolites have shown potential protective effects in preclinical models of OA through anti-inflammatory and antioxidant actions, ECM degradation inhibition, and tissue repair promotion (Figure 2). Notably, recent research has also revealed that garlic-derived exosome-like nanoparticles can attenuate IL-1β-induced ECM degradation, thereby protecting articular cartilage and thus alleviating the progression of OA in vitro and in vivo. This protective effect may result from inhibiting MAPK pathway activation during OA-related inflammation (Liu et al., 2025). Notably, almost all the findings cited in this section are from cell and animal studies, lacking sufficient human clinical evidence. Current data are still insufficient to confirm the clinical efficacy of garlic and its active metabolites in OA treatment. Thus, while preclinical studies suggest that garlic metabolites have potential protective effects, their translational potential for clinical application remains to be validated. Future high-quality human studies, such as well-designed randomized controlled trials, are needed to clarify their efficacy and safety.
The impact of Allicin, SAMC,DAS and DADS on osteoarthritis regulation.
4 The impact of garlic and its active metabolites on osteoporosis regulationOsteoporosis (OP) is a systemic skeletal condition marked by diminished bone mass and deteriorating bone microarchitecture, leading to reduced bone strength and heightened fracture risk. Osteoporosis is classified into two primary categories: primary and secondary. Primary osteoporosis mainly affects the elderly and postmenopausal women (Rachner et al., 2011). OP generally begins around age 40, with a significantly higher incidence in women, particularly as postmenopausal osteoporosis, which is the most prevalent form. In addition to baseline factors like bone volume, strength, and density, the gender difference is mainly due to increased bone turnover and reduced bone density caused by the rapid drop in estrogen levels after menopause. The primary pathological mechanism of OP is the imbalance of bone homeostasis, characterized by disrupted equilibrium between osteoclast-driven bone resorption and osteoblast-driven bone formation. When bone resorption persistently exceeds bone formation, it results in progressive bone loss. Contemporary pathophysiological research has revealed that the process of bone loss involves the complex regulation of various cells, molecules, and signaling pathways. Multiple mechanisms, including hormonal imbalances, dysregulation of pro-inflammatory cytokines, genetic factors, and aging, collectively contribute to the progression of OP, ultimately leading to the destruction of bone microarchitecture, manifested as trabecular microfractures, increased porosity of cortical bone, and a consequent elevation in fracture risk.
4.1 The regulatory effect of garlic oil extract on osteoporosisPostmenopausal osteoporosis is the most prevalent age-related bone loss, primarily resulting from ovarian failure and estrogen deficiency (Yao et al., 2025). Post-menopausal estrogen decline enhances bone resorption via several mechanisms: direct activation of NF-κB signaling in osteoclasts, reduced osteoprotegerin (OPG) expression, increased RANKL/RANK signaling, and diminished estrogen-mediated inhibition of osteoblast apoptosis (Yu et al., 2024). Garlic oil extract has been demonstrated to prevent weight gain and bone loss in ovariectomized mouse models, which simulate ovarian hormone deficiency (Mukherjee et al., 2004). Garlic oil extract effectively mitigates increased osteoclastic activity and bone resorption post-ovariectomy, lowers serum levels of high bone turnover markers like alkaline phosphatase and tartrate-resistant acid phosphatase, and reduces urinary excretion of calcium, phosphorus, and hydroxyproline, indicating a protective effect on bone health. Traditional treatment for postmenopausal osteoporosis involves estrogen replacement therapy or combined estrogen-progestogen therapy. Although this method alleviates menopause-related osteoporosis and its complications, long-term use may increase the risks of embolism or coronary event, stroke, and breast cancer (Bofill Rodriguez et al., 2025). Animal studies indicate that the cholesterol-lowering drugs lovastatin and simvastatin may also have bone-protective properties. Local subcutaneous injection of these two drugs promotes calvarial bone formation in mice, while oral administration increases cancellous bone mass in rats. In vitro experiments have demonstrated that lovastatin inhibits osteoclast formation and attenuates bone damage in mouse models (Mundy et al., 1999). However, statins do not exhibit osteogenic effects at conventional doses, and while high doses exert bone-protective and osteogenic effects, they may induce myotoxicity, hepatotoxicity, and adverse reactions such as gastrointestinal and sleep disturbances, limiting their long-term application (Abdul-Majeed et al., 2012). Preclinical evidence fromovariectomized rat models of osteoporosis suggests that garlic oil extract demonstrates clear anti-osteoporotic potential and benefits for maintaining skeletal health. In these models, garlic oil extract partially restores serum estrogen levels and promotes intestinal calcium transfer, thereby counteracting bone mineral loss caused by ovarian hormone deficiency, a mechanism potentially related to its phytoestrogenic effects (Mukherjee et al., 2006a), (Mukherjee et al., 2006b). Furthermore, garlic may inhibit the progression of bone tissue degeneration in ovariectomized rats by modulating immune cell function, particularly by affecting peritoneal macrophages and lymphocytes involved in the pathogenesis of hypogonadal osteoporosis (Mukherjee et al., 2007).
4.2 The regulatory effects of allicin, alliin, DADS, and DATS on osteoporosisOxidative stress significantly contributes to OP progression by accumulating ROS, which impairs osteoblast function and activates osteoclasts. Allicin enhances bone formation by reducing oxidative stress-induced osteoblast damage through activation of the PI3K/AKT and CREB/ERK signaling pathways, improving mitochondrial function, and inhibiting apoptosis, thereby enhancing bone formation capacity (Ding et al., 2016), (Liu et al., 2020). In contrast, alliin and DADS primarily exert bone-protective effects by inhibiting the aberrant differentiation and function of osteoclasts. Under homeostatic conditions, RANKL from osteoblasts and osteocytes binds to RANK on osteoclasts and their precursors, triggering their activation, fusion, and differentiation into mature multinucleated osteoclasts, thereby increasing bone resorption activity (Armas and Recker, 2012). Concurrently, OPG, produced by osteoblasts and osteogenic stromal stem cells, functions as a decoy receptor for RANKL. OPG competitively binds to RANKL, preventing its interaction with RANK, which inhibits osteoclast differentiation and activation, thus protecting the skeleton from excessive bone resorptionn (Boyce and Xing, 2007), (Yasuda, 2021). However, under inflammatory conditions, an elevated RANKL/OPG ratio and excessive osteoclast activation are observed. Alliin suppresses RANKL-induced osteoclastogenesis and bone resorption by downregulating Nox1 expression, leading to reduced ROS production and inhibition of the c-Fos/NFATc1 signaling pathway (Chen et al., 2016). DADS inhibits osteoclastogenesis by suppressing NF-κB and STAT3 pathways, reducing p65 subunit and STAT3 phosphorylation, and blocking NFATc1 activation and its interaction with NF-κB p65. Simultaneously, DADS decreases the production of pro-inflammatory factors like IL-1β, IL-6, TNF-α, and NO, thereby further inhibiting osteoclast formation (Yang et al., 2019). This dual action of DADS-directly inhibiting osteoclastogenesis and indirectly reducing inflammatory factors-significantly alleviates bone resorption in LPS-induced inflammatory models. DATS enhances mRNA and protein levels of osteogenic factors Runx2 and β-catenin, thereby activating the Wnt/β-catenin signaling pathway for osteogenesis, while concurrently reducing RANKL and TRAF6 expression to suppress osteoclast differentiation. Through these mechanisms, DATS improves trabecular bone microarchitecture, promotes collagen synthesis, and increases bone mineral density and bone volume fraction, thereby exerting anti-osteoporotic effects (Zhang et al., 2023).
Clinical studies further support the potential therapeutic value of garlic and its bioactive metabolites. A study found that garlic tablets with garlic powder and allicin significantly lowered serum levels of pro-inflammatory cytokines, such as TNF-α, IL-1β, and IL-6, in postmenopausal women with osteoporosis. This suggests a potential mechanism for reducing bone loss by inhibiting osteoclastogenesis and extending osteoclast lifespan (de Molon et al., 2018), (Mozaffari-Khosravi et al., 2012). Furthermore, garlic consumption has been shown to decrease levels of oxidative stress biomarkers in postmenopausal women. DAS and DADS, key contributors to garlic’s antioxidant properties, effectively suppress ROS production, restore SOD and GSH-Px activities in osteoblasts, and decrease apoptosis rates, thus improving osteoblast survival under oxidative stress conditions (Ahmadian et al., 2017). The study suggests that garlic and its active metabolites regulate bone metabolism by enhancing osteoblast activity and suppressing osteoclast formation, thus achieving anti-osteoporotic effects through balancing these cell functions.
In summary, garlic and its bioactive metabolites exert multifaceted regulatory effects in the context of osteoporosis by inhibiting osteoclast differentiation and function, enhancing osteoblast activity, and maintaining bone metabolic homeostasis. These effects are facilitated by antioxidant and anti-inflammatory mechanisms, alongside the regulation of critical signaling pathways such as NF-κB/STAT3-NFATc1, PI3K/AKT, and CREB/ERK. These findings provide a novel theoretical basis and potential therapeutic strategies for the treatment of OP (Ahmadian et al., 2017) (Figure 3).
The impact of garlic oil extract, Allicin,Alliin, DADS and DATS on osteoporosis regulation.
5 The impact of garlic and its active metabolites on intervertebral disc degeneration regulationIntervertebral disc degeneration (IVDD) is a progressive and irreversible condition marked by the deterioration of disc tissue, influenced by aging, mechanical stress, genetic factors, and metabolic changes. The intervertebral disc, serving as the shock-absorbing structure of the spine, is a fibrocartilaginous tissue connecting adjacent vertebrae. The intervertebral disc consists of three primary components: the peripheral annulus fibrosus (AF), the central gelatinous nucleus pulposus (NP), and the superior and inferior cartilaginous endplates. The AF is a ring-like structure enveloping the NP and is rich in collagen. The core NP has a gel-like consistency with a water content of 66%–86%, relying on its main ECM components—proteoglycans and type II collagen—to retain water and maintain its gel-like properties (Nedresky et al., 2023). IVDD is characterized by ECM degradation, reduced water and proteoglycan content, AF structural disruption, and diminished NP cell number and function (Yu et al., 2021). This process is often accompanied by enhanced oxidative stress and inflammation (Krut et al., 2021), consequently leading to a decline in the biomechanical properties of the intervertebral disc. Structural changes such as intervertebral space narrowing, osteophyte formation, annulus fibrosus fissures, and disc herniation can lead to clinical manifestations like low back pain and spinal stenosis (Xin et al., 2022).
The core pathological mechanism of IVDD is an imbalance between ECM synthesis and degradation within the NP. Oxidative stress and inflammation are key drivers in the progression of IVDD, triggered by factors like genetics, aging, and mechanical loading (Lu et al., 2023), (Chen et al., 2025), (Zhang et al., 2025), (Sao and Risbud, 2024). The intervertebral disc tissue primarily relies on anaerobic glycolysis for energy production (Wu et al., 2021), (Kim et al., 2021), a metabolic state that inherently predisposes it to increased ROS generation (Li et al., 2020). As age increases and IVDD progresses, the disc’s endogenous antioxidant defense system deteriorates, resulting in mitochondrial dysfunction and ROS accumulation (Chen et al., 2024). The excessive accumulation of ROS activates a series of MMPs and inhibits the expression of TIMPs, thereby accelerating ECM degradation. Direct evidence from IVDD-specific models indicates that allicin may protect against disc degeneration. Allicin has been shown to reduce oxidative stress and mitochondrial apoptosis in NP cells (Xi et al., 2020). Subsequent studies demonstrated that an ROS-responsive hydrogel containing allicin effectively prevents NP cell apoptosis and ECM degradation, while enhancing NP cell growth, proliferation, and repair. In animal models, this treatment significantly delayed IVDD and maintained disc morphology and matrix integrity (Zhang et al., 2025). In the study’s cellular experiments, H2O2 treatment significantly decreased Bcl-2 expression while increasing Bax, caspase-3, and caspase-9 levels, thus inducing apoptosis. Allicin treatment reversed the alterations in protein expression. The results indicate that allicin could slow IVDD progression by safeguarding NP cells against apoptosis caused by oxidative
Comments (0)