Anti-inflammatory and anti-osteoarthritis effects of tectorigenin

Abstract

Osteoarthritis (OA) is a common and dynamic disease of the joints, including the articular cartilage, underlying bones and synovium. In particular, OA is considered as the degeneration of the cartilage. Tectorigenin (Tec) is known to affect many biological processes; however, its effects on articular chondrocytes remain unclear. This study aimed to assess the effects of Tec on articular cartilage. In vitro, Tec inhibited the expression levels of type X collagen, cyclooxigenase-2, matrix metalloproteinase (MMP)-3 and MMP-13, but enhanced the expression of Runx1, type II collagen and aggrecan in the presence of IL-1β. Meanwhile, Tec inhibited apoptosis through the Bax/Bcl-2/caspase-3 pathway, upregulating p-Bad, downregulating the Bax/Bcl-2 ratio, and activating caspase-3 compared with IL-1β treatment only. Moreover, this process was partially regulated by NF-κB P65. In vivo, the chondroprotective effects of Tec were assessed by establishing a model of surgically induced OA. Tec-treated joints exhibited fewer osteoarthritic changes than saline-treated joints. Meanwhile, 1.5 μg/kg Tec treatment produced a greater protective effect than 0.75 μg/kg Tec. The Osteoarthritis Research Society International (OARSI) scoring system, employed to assess histopathological grading of the models, as well immunohistochemistry for Aggrecan Neoepitope and MMP-3, further confirmed the results. In conclusion, this study showed that Tec plays a chondroprotective role in the OA process by preventing articular cartilage degeneration and chondrocyte apoptosis via the NF-κB P65 pathway.

Tectorigenin protects against experimental fulminant hepatic failure by regulating the TLR4/mitogen‐activated protein kinase and TLR4/nuclear factor‐κB pathways and autophagy

“…Tectorigenin (Tec; Figure a), a component of Belamcanda Adans, has antiproliferation, anti‐inflammatory, and antioxidant activities (Wang et al, ). Presently, the main studies on Tec have focused on its antitumor effects via the NF‐κB and MAPK pathways (Yang et al, ; Zeng et al, ).…”

Tectorigenin inhibits RANKL‐induced osteoclastogenesis via suppression of NF‐κB signalling and decreases bone loss in ovariectomized C57BL/6

“…22,25 It has been reported in other studies that tectorigenin inhibit activation of NF-κB on other cells. 15,26,27 In this study, we evaluated the activation of NF-κB signalling in the tectorigenin treatment on BMM cells. Our data demonstrated that tectorigenin could inhibit degradation of IκBα and phosphorylation of NF-κB p65…”

“…Its potential usage in anti-inflammatory and antioxidant activity was reported before, 13,14 and more specifically, its anti-inflammatory effect in osteoarthritis and NF-κB signalling blockage. 15 In this study, the effect of tectorigenin on RANKL-induced NF-κB activation and osteoclastogenesis was investigated in vitro, plus its anti-osteoporosis action in an ovariectomized (OVX) mice model. β-actin (SC-47778) antibodies was purchased from Santa Cruz Biotechnology.…”

Recent advance in treatment of osteoarthritis by bioactive components from herbal medicine

“…In OA chondrocytes, resveratrol may reverse the decrease in the levels of type II collagen, aggrecan, and glycosaminoglycan by regulating silent information regulator 2 type 1, hypoxia-inducible factor-2α, and MMPs expression [24,62,63,77]. Curcumin [28], naringin [42], icariin [16,78,79], berberine [68,69], sinomenine [72], tetramethylpyrazine [13,70,80], astragaloside IV [81], halofuginone [82], puerarin [83], quercetin [84], celastrol [54,85], harpagoside [32], ferulic acid [55], shikonin, acetylshikonin [86], ginsenoside Rb1 [76,87], cinnamophilin [30], honokiol [50], 2, 3, 5, 4′-tetrahydroxystilbene-2-O-β-d-glucoside [60], geniposide [31], ginsenoside Rg5 [74], cryptotanshinone [29], isofraxidin [33], paeonol [56], crocin [43], coptisine [44], piperine [45], butein [46], licochalcone A [36], tectorigenin [48], theaflavin-3,3′-digallate [59], anemonin [49], gastrodin [51], compound K…”

“…Emodin ameliorates OA cartilage inflammation by inhibiting NF-κB and Wnt/β-catenin signaling [ 38 , 39 ]. NF-κB signaling pathway is also involved in the treatment of cartilage inflammation by icariin [ 40 , 41 ], arasaponin R1 [ 41 ], berberine [ 17 ], tetramethylpyrazine [ 13 ], naringin [ 42 ], crocin [ 43 ], coptisine [ 44 ]; piperine [ 45 ], butein [ 46 ]; kaempferol [ 47 ], tectorigenin [ 48 ], anemonin [ 49 ], honokiol [ 50 ], and gastrodin [ 51 ]. In addition, some molecules have been reported to reduce the expression of inflammatory factors in OA cartilage, but the related pathways still need to be further explored, such as astragaloside IV [ 52 ], puerarin [ 53 ], celastrol [ 54 ], ferulic acid [ 55 ], paeonol [ 56 ], artesunate [ 57 ], genistein [ 58 ], theaflavin-3,3′-digallate [ 59 ], and 2, 3, 5,4′-tetrahydroxystilbene-2-O-β- d -glucoside [ 60 ].…”