Vernonia amygdalina inhibited osteoarthritis development by anti‐inflammatory and anticollagenase pathways in cartilage explant and osteoarthritis‐induced rat model

Abstract

Vernonia amygdalina (VA) is a medicinal tropical herb for diabetes and malaria and believed to be beneficial for joint pains. The antiosteorthritis effects of VA leaf in cartilage explant assays and on postmenopausal osteoarthritis (OA) rat model were investigated. The VA reduced the proteoglycan and nitric oxide release from the cartilage explants with interleukin 1β (IL‐1β) stimulation. For the preclinical investigation, ovariectomized (OVX) female rats were grouped (n = 8) into nontreated OA, OA + diclofenac (5 mg/kg), OA + VA extract (150 and 300 mg/kg), and healthy sham control. Monosodium iodoacetate was injected into the knee joints to accelerate OA development. After 8 weeks, the macroscopic, microscopic, and histological images showed that the OA rats treated with VA 300 mg/kg and diclofenac had significantly reduced cartilage erosions and osteophytes unlike the control OA rats. The extract significantly down‐regulated the inflammatory prostaglandin E2, nuclear factor κβ, IL‐1β, ADAMTS‐5, collagen type 10α1, and caspase3 in the OVX‐OA rats. It up‐regulated the anti‐inflammatory IL‐10 and collagen type 2α1 mRNA expressions, besides reducing serum collagenases (MMP‐3 and MMP‐13) and collagen type II degradation biomarker (CTX‐II) levels in these rats. The VA (containing various caffeoyl‐quinic acids, flavanone‐O‐rutinoside, luteolin, apigenin derivative and vernonioside D) suppressed inflammation, pain, collagenases as well as cartilage degradation, and improved cartilage matrix synthesis to prevent OA.

Polysaccharide from angelica sinensis attenuates SNP-Induced Apoptosis in osteoarthritis Chondrocytes by Inducing Autophagy via ERK1/2 Pathway

“…In addition, synovial cells and cartilage cells in OA produce large amounts of NO [21]. The negative effects of NO include enhancement of matrix metalloproteinase activity, a reduction in interleukin-1 receptor antagonist synthesis and the promotion of apoptosis, which are closely associated with the occurrence and development of OA [22][23][24]. Thus, we chose SNP to induce NO-related apoptosis, and discovered that chondrocyte viability declined in a time and dose-dependent manner.…”

Polysaccharide from Angelica sinensis attenuates SNP-induced apoptosis in osteoarthritis chondrocytes by inducing autophagy via ERK1/2 pathway

“…In addition, synovial cells and cartilage cells in OA produced large amounts of NO [23]. The negative effects of NO include enhancement of matrix metalloproteinase activity, a reduction in interleukin-1 receptor antagonist synthesis and the promotion of apoptosis, which are closely associated with the occurrence and development of OA [24][25][26]. Thus, we chose SNP to induce NO-related apoptosis, and discovered that chondrocyte viability declined in a time and dose-dependent manner.…”

Polysaccharide from angelica sinensis attenuates SNP-Induced Apoptosis in osteoarthritis Chondrocytes by Inducing Autophagy via ERK1/2 Pathway

“…In addition, synovial cells and cartilage cells in OA produce large amounts of NO [23]. The negative effects of NO include enhancement of matrix metalloproteinase activity, a reduction in interleukin-1 receptor antagonist synthesis and the promotion of apoptosis, which are closely associated with the occurrence and development of OA [24][25][26]. Thus, we chose SNP to induce NO-related apoptosis, and discovered that chondrocyte viability declined in a time and dose-dependent manner.…”