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V. BaradaranRahimi and V. R. Askari

[72]

↓ ESR level

[73]

↓CRP level

↑ number of patients with at least 20%,

50%, and 70% improvement in disease

activity

[74]

↓ number of swollen and tender joints

↓ IL-6 and rheumatoid factor levels

↓ IgG, IgA, IgM, CRP, IL-6, and TNF-α

levels

↑ patients satisfaction degree

↓ lower rate of adverse effects

[75]

↓ morning stiffness, tender and swollen

joint count

[76]

↓ VAS pain score

↓ CRP, ESR, and rheumatoid factor

levels

↓ DAS28, number of swollen joints,

[77]

tender joints, and pain intensity

↓ HAQ score, morning stiffness

↓ ESR level

↑ GPx level

↓ knee pain, swelling

[78]

↑ knee exion and walking distance

↓ WOMAC index, VAS pain score,

European Q5D quality of life

↓hs-CRP level

[79]

↑ 6-min walk test score

↑ joint space

↓ osteophytes

↓ DAS28ESR disease activity score

[80]

↓ number of tender and swollen joints,

VAS pain score, DAS28 score

↑ physician global assessment

↓hs-CRP, TNF-α, IFN-γ, and MDA

levels

↑ Total anti-oxidant capacity

[81]

↓ VAS pain score

↓IL-17 and CRP levels

↑ T reg cells

↓ T helper 17 cells

A meta-analysis of six clinical studies

involving 438 patients with RA and

ulcerative colitis

A randomized, controlled trial on

rheumatoid arthritis patients

• 250 to 1500mg/day for 8–12weeks

• Placebo

24weeks

• 60mg three times daily

• Sulfasalazine 1g twice daily taken for

A randomized, controlled trial on

rheumatoid arthritis patients

months

daily + methotrexate 7.5mg once a week

• Tripterygium wilfordii10mg three times

• Methotrexate 15mg once a week for 3

A meta-analysis of 40 clinical studies

involving 3092 RA patients

• T.Wilfordii + methotrexate

• Methotrexate monotherapy

A double-blind, randomized clinical trial on

RA patients

• 250mg twice a day over 8 weeks

• Placebo

A randomized, double-blind, placebo-

controlled crossover trial on patients with

• 333mg three times per day over 8 weeks

• Placebo

knee osteoarthritis

A pilot, randomized, double-blind,

placebo-controlled trial on knee

osteoarthritis patients

• 169.33mg two times a day for 120days

• Placebo

A double-blind, placebo-controlled,

randomized trial on RA patients

90days

• 100mg/day (pure saffron powder) for

• Placebo

A randomized, double-blind, placebo-

controlled clinical trial on RA patients

• 100mg/day taken over 12weeks

• Placebo

A randomized, double-blind, placebo-

controlled clinical trial on osteoarthritis

patients

• 15mg/day for 4 months

• Placebo

Extract type or plant part Study design Study model Results Ref

Curcumin

Table 2 (continued)

Tripterygium wilfordii

Punica granatum

Boswellia serrata

Crocus sativus

Crocin

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281

[82]

↓ microRNA-21 gene expression levels

↑ microRNA-155 gene expression levels

[83]

↓ modied WOMAC score, knee

swelling index

↓ VAS pain score, stiffness, and

disability

[84]

↓ WOMAC pain, stiffness, dysfunction

score

↓ BGP, S100A12, IL-17, and SIP levels

A randomized, double-blind, placebo-

controlled clinical trial on osteoarthritis

patients

A randomized, double-blind, placebo-

controlled on patients with knee

osteoarthritis

A clinical study evaluating patients with

osteoarthritis and osteonecrosis

• Placebo

12weeks

• 125 and 250mg twice a day over

• Placebo

meloxicam

• Meloxicam

Extract type or plant part Study design Study model Results Ref

Crocin • 15mg/day for 4months

Aqueous extract of roots and

leaves of Withania somnifera

Eucommia ulmoides granules • 12g three times a day for 1month +

box P3, GAT A3 GATA binding protein 3, PPAR-γ peroxisome proliferator-activated receptor gamma, VAS visual assessment scale, BGP bone-GLA protein, S100A12 recombinant human S100

calcium-binding protein, SIP sphingosine 1-phosphate

hs-CRP high sensitivity C-reactive protein, MDA malondialdehyde, NO nitric oxide, IL interleukin, T-bet T-box transcription factor TBX, RORγt RAR-related orphan receptor γt, FoxP3 forkhead

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2.1 Animal Studies

In streptococcal cell wall (SCW)-induced arthritis, Z. ofcinale extract and essential oil rmly decrease arthritic index,

joint swelling, and cartilage destruction index in female rats [6, 7]. In addition, Z. ofcinale rhizomes powder remarkably alleviated paw edema, TNF-α, IL-1β, -6, and 4 levels while elevating IL-10 levels following CFA-induced arthritis in rats [8].

Seventy percent of hydroethanolic extract of Z. ofcinale rhizomes meaningfully reduced clinical scores, arthritic incidence, erythrocyte sedimentation rate (ESR) level, joint temperature, joint swelling, and destruction of cartilage following CIA. Z. ofcinale also mitigated the serum levels of IL-1β, -6, and -2, TNF-α, and anti-CII antibodies following CIA in rats [9].

2.1.1 6-Shogaol

6-Shogaol notably alleviated paw volume, activities of lysosomal enzymes, lipid peroxidation, as well as TNF-α level while enhancing glutathione peroxidase (Gpx), SOD, and CAT activities in gouty arthritis associated with monosodium urate crystal administration in mice [10]. Moreover, 6-shogaol signicantly inhibited knee swelling and edema, leukocyte inltration into the synovial cavity, and VCAM-1 level in CFA-induced arthritis in rats [11].

2.2 Clinical Studies

Z. ofcinale rhizomes powder remarkably decreased DAS28 arthritis score, T-bet, NF-κB, and RORγt gene expression in RA patients. It also stimulated the forkhead box P3 (FoxP3), GATA binding protein 3 (GAT A3), and peroxisome proliferator-activated receptor gamma (PPAR-γ)in RA patients [64].

Z. ofcinale rhizomes powder strikingly mitigated visual assessment scale (VAS) pain score while improving satisfaction with treatment in patients with knee osteoarthritis [65]. Similarly, 95% hydroethanolic extract of Z. ofcinale markedly reduced VAS and gelling pain scores in patients with osteoarthritis [66]. Additionally, Z. ofcinale powder provided a signicant decrement in VAS pain score, WOMAC pain score, morning stiffness, as well as difculty in knee osteoarthritis patients [67].

3 Curcuma longa andIts Major Active

Constituent Curcumin

Curcuma longa (C. longa), popularly named turmeric, is a perennial rhizomatous herb and member of Zingiberaceae. It is cultivated chiey in Asia, India, Iran, and China. Curcumin

is the major and well-studied polyphenol isolated from the rhizome of C. longa. Curcumin possesses plenty of promising impacts, namely anti-oxidant, anti-inammatory, immunomodulatory, antimicrobial, anti-cancer, neuroprotective, and anti-arthritis effects [92, 93].

3.1 Animal Studies

In the CIA model, curcumin meaningfully decreased arthritis score, joint histopathological changes, levels of TNF-α, IL-17 and 1β, and TGF-β, degradation of IκBα, and COX-2 expression in the synovium of the rat joints [12]. Similarly, curcumin markedly diminished clinical score, histology score, matrix metalloproteinases (MMP)-1, 3, 9, and 13 protein expression, and anti-collagen type II antibodies following CIA.It also diminished inammatory markers, including TNF-α, IL-1β, 6, 33, 15, and 16, IFN-γ, IFN-gammainducible protein 10 (IP-10), macrophage inammatory proteins (MIP)-α, and monocyte chemoattractant protein-1 (MCP-1) in CIA mice [13].

Curcumin notably mitigated redness and paw edema, arthritis score, inammatory cells permeation into the synovium, and TNF-α, IL-1β, MMP-1, and 3 levels in serum and synovium following CIA in rats. It also suppressed mTOR, p70S6 kinase, and eukaryotic initiation factor 4E binding protein 1 expression in the synovium of CIA rats [14]. Additionally, curcumin remarkably alleviated arthritis scores, paw edema, TNF-α, IL-6, IL-17, phospho(phosphoinositide-3 kinase) p-PI3K/PI3K ratio, and p-AKT/ AKT ration in CIA in mice [15].

In CFA-induced arthritis in rats, curcumin signicantly propagated SOD, CAT, and Gpx activities, and methionine sulfoxide reductase A (MSRA)gene expression [16].

In the model of knee osteoarthritis caused by monosodium iodoacetate (MIA) in rats, curcumin strikingly mitigated TNF-α, IL-1β, MMP-3, cartilage oligomeric matrix protein (COMP) while elevated SOD, and collagen II levels. It also inhibited the TLR4/NF-κB signaling pathway by suppressing TLR4, cox-2, and p-p65 expression levels [17]. Furthermore, curcumin stimulated the number of chondrocytes, collagen 2, SOX-5, and Indian hedgehog (IHH) expression in zymosan-induced osteoarthritis in rats [18].

In monosodium urate (MSU)-induced acute gout in mice, curcumin rmly attenuated paw and ankle joint swelling, MPO activity, and p-p65 and p-p50 phosphorylation while enhancing IκBα protein levels. It also provided a signicant decrement in COX-2, TLR4, myeloid differentiation factor 88, and NLRP3 expression in the footpad tissue [19]. Similarly, curcumin considerably prevented ankle circumference, penetration of neutrophils in knee joints, TNF-α, IL-1β, and elastase levels in MSU-induced acute gout in rats. In addition, curcumin suppressed the levels of NLRP3, pro-

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283

Fig. 2 The anti-arthritis mechanisms of Curcuma longa and its main active ingredient curcumin. TLR4 toll-like receptor 4, NF-κB nuclear factor-κB, SOD superoxide dismutase, CAT catalase, Gpx glutathione peroxidase, NLRP3 NLR family pyrin domain containing3, MMP

caspase- 1, caspase-1, pro-IL-1β, and IL-1β in the rat knee joints [20].

3.2 Clinical Studies

Curcumin signicantly decreased VAS pain score and the need for NSAID consumption in patients with knee osteoarthritis [68]. Interestingly, curcumin indicated similar effects to diclofenac in bettering pain and quality of life in knee osteoarthritis patients. However, curcumin was better tolerated and had signicantly lower adverse effects compared to diclofenac [94]. Additionally, curcumin with diclofenac remarkably diminished pain, the need for rescue analgesics, the need for histamine 2 (H2) blockers, and fewer side effects compared to diclofenac consumption in patients with knee osteoarthritis [69]. Recently, a meta-analysis of 20 clinical studies involving 1927 patients with osteoarthritis emphasized that curcumin markedly attenuated VAS pain score, WOMAC-pain, physical function and stiffness, ESR level, and oxidative stress markers while elevating anti-oxidative stress markers [70].

Curcumin also possesses anti-inammatory and analgesic

impacts in RA patients. In this regard, curcumin meaning-

matrix metallopeptidase, mTOR mammalian target of rapamycin, IL interleukin, TNF-α tumor necrosis factor-α, TGF-β1 transforming growth factor-β1, IFN-γ interferon-gamma, PI3K phosphoinositide-3 kinase

fully alleviated VAS pain score, DAS 28 score, rheumatoid factor values, CRP, and ESR levels in RA patients [71]. Additionally, Zeng and coworkers conducted a meta- analysis of six clinical studies evaluating 326 patients with RA.They noticed that curcumin signicantly mitigated the DAS 28 score, rheumatoid factor values, ESR, and CRP levels [70]. Another meta-analysis investigated six clinical studies involving 438 patients and showed that curcumin notably decreased ESR and CRP levels in rheumatoid arthritis and ulcerative colitis patients [72].

Taken together, curcumin ameliorated the severity of pain and inammation along with safety in RA and osteoarthritis patients (Fig.2).

4 Tripterygium wilfordii Hook andIts Main

Component Triptolide

Tripterygium wilfordii Hook (T. wilfordii), commonly named as thunder god vine, is a traditional Chinese plant belonging to Celastraceae. The whole plant may cause acute toxicity, and its roots are the medicinal part of the plant. Triptolide is the major active diterpenoid isolated from the roots of T. wil- fordii. Several pieces of evidence support that T. wilfordii

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and triptolide may be benecial in treating inammatory and auto-immune disorders, such as RA, multiple sclerosis, Lupus, psoriasis, diabetic nephritic syndrome, and Behcet’s disease [95, 96].

4.1 Animal Studies

In CIA in rats, total alkaloids of T. wilfordii signicantly decreased paw swelling, TNF-α, IL-6 and 8, and NF-κB levels in serum and synovial tissue [21]. Similarly, T. wilfordii glycosides markedly diminished paw volume, arthritis score, histopathological damages, anti-typeIIcollagen antibodies, and IL-1β levels in CIA rats [22].

4.1.1 Triptolide

In CIA in rats, triptolide notably mitigated paw thickness, arthritis score, levels of MPO, COX-2, iNOS, and oxidative stress in the articular tissue [23]. Similarly, triptolide considerably reduced arthritis score, TNF-α, IL-1β and 6, MMP-3 and -9, unconventional prefoldin RPB5 interactor 1, frequently rearranged in advanced T cell lymphomas-1 mRNA expression in synovial tissue of CIA rats [24]. Zou et al. noticed that the anti-arthritis properties of triptolide are through activating PI3K/AKT signaling cascade while inhibiting VEGF and tumor necrosis factor-related protein 3in adjuvant arthritis model in rats [25].

In TNF transgenic mice with RA, triptolide rmly alleviated arthritis score, TNF-α, IL-1β, and IL-α levels while elevating arthritis detumescence percentages and apoptosis rates of osteoclast precursor cells (OCP) and T lymphocytes [26]. Similarly, triptolide meaningfully decreased arthritis symptoms, joint swelling, osteoclast (OC) cell levels, inammation, swelling, and bone erosion while stimulating the rate of apoptosis in OCP cells in TNF transgenic mice [27].

improved the patient’s satisfaction degree while having a lower rate of adverse effects than methotrexate monotherapy [74].

Additionally, several systematic reviews and metaanalysis studies determined the effects of T. wilfordii in RA patients. In this regard, two studies supported that T. wilfordii signicantly improved grip strength, swelling joint count, morning stiffness, CRP, rheumatoid factor, ESR levels, and risk of adverse events than the placebo and methotrexate monotherapy [98, 99]. Similarly, a meta-analysis of 40 clinical studies involving 3092 RA patients emphasized that combination therapy of T. wilfordii and methotrexate notably alleviated morning stiffness, tender and swollen joint count, VAS pain grade, CRP, ESR, and rheumatoid factor levels compared to methotrexate monotherapy [75].

In general, T. wilfordii extract and its main constituent, triptolide, may be promising agents for treating RA patients.

5 Punica granatum andIts Major

Constituent Ellagic Acid

Punica granatum (P. granatum), universally famous as pomegranate, is a small deciduous tree belonging to Punicaceae. Pomegranate is mainly cultivated in the Mediterranean countries, namely India, Iran, Turkey, and China. Multiple pharmacological effects have been emphasized for P. granatum fruit, namely anti-oxidant, anti- inammatory, antidiabetic, hepatoprotective, cardioprotective, and anti-arthritis activities [100, 101]. In addition, ellagic acid (EA) and punicalagin are the major and well-studied active polyphenolic compounds found in pomegranate fruits [102, 103].

5.1 Animal Studies

4.2 Clinical Studies

T. wilfordii extract remarkably propagated the number of patients with at least 20%, 50%, and 70% improvement in disease activity compared to the sulfasalazine group in RA patients. Moreover, T. wilfordii extract notably decreased swollen and tender joint numbers, IL-6, and rheumatoid factor levels in RA patients [73]. In contrast, Zhou and coworkers suggested that T. wilfordii extract was not inferior to methotrexate treatment in RA patients [97].

Han and co-workers investigated the effects of combination therapy of total glycosides of T. wilfordii and methotrex- ate. They showed that T. wilfordii plus methotrexate treatment meaningfully diminished IgG, IgA, IgM, CRP, IL-6, and TNF-α levels in RA patients. In addition, T. wilfordii also

In the CFA-induced arthritis model, P. granatum rind extract signicantly decreased paw volume, histopathological damage, MPO activity, TNF-α, and IL-1β levels [28]. Similarly, P. granatum rind extract notably reduced paw volume, MDA, TNF-α levels, TNF receptor 1 (TNF-R1), TNF-α, IL-1β and 6, and NF-κB expression while increasing GSH levels and SOD activity in the synovial joint following CFA-caused arthritis in rats [29].

Following CFA-induced arthritis in rats, ethanolic extract of P. granatum markedly diminished paw volume, arthritic score, histological damages, MDA, rheumatoid factor (RF), TNF-α, and IL-1β levels [30]. Similarly, the P. granatum extract meaningfully alleviated the arthritic score, paw volume, joint diameter, as well as level of ESR [31].

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Fig. 3 The anti-arthritis mechanisms of Punica granatum and its main active constituents, EA and Punicalagin. MDA malondialdehyde, NO nitric oxide, SOD superoxide dismutase, GSH glutathione, CAT catalase, iNOS inducible nitric oxide synthase, IL interleukin, TNF-α tumor

5.1.1 Ellagic Acid (EA)

In arthritis induction by adjuvant in mice, EA markedly decreased paw edema, histopathological damage, TNF-α, IL-1β, and IL-17 levels while increasing IL-10 and IFN-γ levels [32]. Similarly, EA signicantly mitigated paw edema, chitinase-3-like protein-1 (CHI3L1), NF-κB, IL-1β, MMP-9, VEGF, and Caspase-3 expression in rats. Moreover, EA provided a signicant reduction in oxidative stress markers while enhancing GSH levels following adjuvant-caused arthritis in rats [33].

In CFA-induced arthritis, EA notably alleviated paw swelling, arthritis index, pathological damages, and synovial tissue levels of TNF-α, IL-1β , and 6. Additionally, EA downregulated the expression of metastasis-associated gene (MTA)-1 and histone deacetylase 1 while up-regulating Nur77in CFA-induced arthritis in rats [34].

5.1.2 Punicalagin

In CIA in mice, punicalagin markedly attenuated paw volume, clinical arthritis score, histology score, TNF-α, and IL-6 levels [35]. Similarly, punicalagin considerably decreased paw thickness, arthritis score, and bone destruction. Furthermore, punicalagin changed the phenotype of macrophages from M1 to M2 through diminishing iNOS, TNF-α, IL-1β, and IL-6 while stimulating arginase-1 (Arg-1)

necrosis factor-α, MMP matrix metallopeptidase, VEGF vascular endothelial growth factor, IFN-γ interferon-gamma, ESR erythrocyte sedimentation rate, NF-κB nuclear factor-κB

and IL-10 expression. Punicalagin also provided a signicant decrement in the expression of NLRP3 and caspase-1in the joint synovial membrane of CIA mice [36].

5.2 Clinical Studies

P. granatum extract signicantly attenuated DAS28, swollen joint numbers, tender joints, and pain intensity in RA patients. Additionally, P. granatum extract meaningfully diminished HAQ score, morning stiffness, and ESR level while propagating GPx level in RA patients [76].

Collectively, P. granatum extract and its main constitu- ents, EA and punicalagin, may be promising candidates for improving arthritis (Fig.3).

6 Boswellia serrata andIts Major

Constituent Boswellic Acid

Boswellia serrata (B. serrata), commonly called Indian frankincense, is a branching tree member of Burseraceae. Chiey, B. serratais native to India, and the oleo gum-resins are the most used part of the plant. B. serrata possesses antiinammatory properties and is frequently used to treat RA

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and osteoarthritis. In addition, boswellic acid is the major and well-studied active constituent of B. serrata [104, 105].

6.1 Animal Studies

In CIA model, extract of B. serrata gum resin notably decreased paw diameter, clinical severity score, elastase, and levels of MPO, MDA, and NO while enhancing GSH level, SOD, and CAT activities in joints. It also attenuated inammatory markers, including TNF-α, IL-1β and 6, IFN-γ, and PGE2, while stimulating IL-10 levels in CIA in rats [37]. Similarly, B. serrata extracts markedly alleviated arthritis index, paw volume, pain, motility score, stair climbing, and histopathological damages in CIA rats. Moreover, B. serrata meaningfully attenuated collagen antibodies, CRP, and ESR levels in serum while elevating the synovial uid levels of hyaluronan and cartilage oligomeric matrix protein (COMP) in CIA rats [38].

In CFA-induced arthritis in rats, B. serrata gum resin extract notably diminished ankle diameter and arthritis index while improving body weight [106].

6.1.1 Boswellic Acid

Boswellic acid signicantly ameliorated carrageenan and Mycobacterium-caused paw edema and arthritis in rats. Interestingly, the promising anti-arthritis effects of boswellic acid were signicantly greater than glucosamine. Additionally, combination therapy of boswellic acid and glucosamine showed synergistic effects in chronic arthritis models in rats [107]. Similarly, boswellic acid considerably alleviated paw edema, ESR, and MDA levels while increasing anti-oxidant enzymes following CFA-induced arthritis in rats [40].

In the gouty arthritic model following monosodium urate crystal administration in mice, boswellic acid remarkably reduced paw thickness, lysosomal enzymes, MDA, and TNF-α levels. Furthermore, boswellic acid also enhanced SOD, GPx, and CAT activities in gouty arthritis mice [39].

6.2 Clinical Studies

B. serrata extract signicantly alleviated knee pain and swelling while elevating knee exion and walking distance in patients with knee osteoarthritis. Additionally, no signicant adverse effects were observed following B. serrata extract treatment, and it was well tolerated [77]. Similarly, B. serrata extract remarkably mitigated WOMAC index, VAS pain score, European Q5D quality of life, and hs-CRP level while promoting a 6-min walk test score in knee osteoarthritis patients. Furthermore, the benecial effects of B. serrata extract have been conrmed by radiographic assessments

showing an increment in joint space and a decrement in osteophytes. They also reported no serious adverse events following treatment with B. serrata extract [78].

Taken together, B. serrata and its main constituent boswellic acid may be effective in improving RA and osteoarthritis.

7 Crocus sativus andIts Main Constituent

Crocin

Crocus sativus (C. sativus), universally famous as saffron, is a perennial owering plant and member of Iridaceae. The red ower stigmas of C. sativus are known as saffron spice or red gold, widely used as spice and preparing food colorant in foods worldwide. Crocin is considered the main active and well-studied component of C. sativus. Several pieces of evidence support that C. sativus and crocin have anti-oxidant, anti-inammatory, anti-depressant, analgesic, and antiarthritis effects [108, 109].

7.1 Animal Studies

7.1.1 Crocin

In CFA-induced arthritis in rats, crocin markedly reduced paw swelling, exoglycosidases, Cathepsin-D, alkaline phosphatase, acid phosphatase, and tartrate-resistant acid phosphatase activities. It also mitigated inammatory biomarkers, namely TNF-α, IL-1β and 6, NF-kB, cyclooxygenase-2, and PGE2. Besides that, crocin provided a meaningful suppression in reactive oxygen species (ROS) while enhancing antioxidative markers in CFA-induced arthritis in rats [41]. Similarly, crocin strikingly mitigated paw swelling, arthritis score, levels oNOS, NO, TNF-α, IL-1β, and 6 in CFAinduced arthritis in rats [42].

In CIA in mice, crocin notably alleviated arthritis score, paw thickness, histological score, MMP-1, -3, and -13, TNFα, IL-6, -17, and -8, and CXCL8 levels [43]. Similarly, cro- cin signicantly reduced mean clinical score, TNF-α, IL-1β, and -6 levels following CIA in mice [44].

In adjuvant-caused arthritis in rats, crocin markedly diminished pain, TNF-α and IL-1β levels. Crocin also suppressed the Wnt5a/β-Catenin Pathway and glial activation by decreasing the levels of GFAP and Iba-1in the spinal cords of AIA rats [45].

In meniscectomy surgery-induced osteoarthritis, crocin rmly alleviated joint pain, ROS, lipid peroxidation, and JNK levels while enhancing GSH and GPx activities. Crocin also improved muscle dysfunction by reducing muscular levels of IL-6, citrate synthase activity, and myosin heavy chain IIα in osteoarthritis rats [46].

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7.2 Clinical Studies

C. sativus signicantly reduced DAS28ESR disease activity score in RA patients following 90days of treatment [79]. Similarly, C. sativus notably diminished the number of tender and swollen joints, VAS pain grade, and DAS28 score while improving physician global assessment in RA patients. It also mitigated hs-CRP, TNF-α, IFN-γ, and MDA levels while enhancing total anti-oxidant capacity in RA patients [80].

Additionally, crocin remarkably diminished VAS pain score, CRP, and IL-17 levels in osteoarthritis patients. Crocin also elevated the percentage of T regulatory (Tregs) while decreasing T helper (Th) 17 cells in osteoarthritis patients. In fact, crocin shifted the Treg/Th17 ratio toward Treg cells in osteoarthritis patients [81]. Similarly, crocin attenuated the microRNA-21 gene expression levels while stimulating microRNA-155 gene expression levels in osteoarthritis patients [82].

In general, C. sativus and its main ingredient, crocin, may be a promising candidate for treating RA and osteoarthritis.

8 Berberis vulgaris andIts Main

Constituent Berberine

Berberis vulgaris (B. vulgaris), commonly known as barberry, is a deciduous shrub and member of Berberidaceae. The edible part of B. vulgaris is its oblong red fruit with a sour avor. Its fruits are frequently used for cooking and making jams in different countries worldwide. The main and well-studied active constituent of the plant is berberine. B. vulgaris and berberine showed anti-inammatory, antioxidant, analgesic, and anti-arthritis properties [110, 111].

8.1 Animal Studies

8.1.1 Berberine

In CFA-induced arthritis in rats, berberine considerably reduced paw swelling, arthritis index score, IL-6, IL-17, and anti-IL-17 antibodies while elevating IL-10, TGF-β, and anti-IL-10 antibodies [47].

In CFA-caused arthritis, berberine remarkably diminished paw swelling, arthritis global assessment, and histopathological damages in rats. Berberine also regulated M1/M2 balance by attenuating the M1 markers, namely, TNF-α, iNOS, and IL-1β and -6 while elevating the M2 markers, including IL-10, TGF-β1, and Arg1. Moreover, berberine alleviated the Th17/Treg cells ratio by decreasing the number of Th17 while increasing Treg cells. In addition, berberine stimulated the p-AMPK expression while downregulated p-p65, p-IκBα, and COX-2 expression in CFA-induced arthritis in rats [48]. Similarly, berberine suppressed the inammatory marker levels (TNF-α, IL-1β, -6, and -17, MCP-1, and IFN-γ) as well as the proportion of M1 macrophages. In contrast, it propagated the levels of antiinammatory indicators, such as IL-10 and -4, and TGF-β1 as well as the proportion of M2 macrophages in CFA-caused arthritis. Additionally, berberine up regulated p-AMPK expression while diminishing HIF-1α expression in synovial macrophages [49].

In CIA in mice, berberine leads to T cell suppression through attenuating the number of CD4+Th, CD4+CXCR5+Tfh cells, CD28, CD154 expression, and anti-CII total IgG serum levels while enhancing Foxp3+ Treg cells [50]. Similarly, berberine markedly diminished paw swelling, arthritis index, histological score, joint destruction, RANKL, TNF-α, IL-1β, and IL-6in CIA in rats. Berberine prevented the proportion of Th17 cells, IL-17 levels, and phosphorylation of STAT3 [51]. Similarly, berberine notably alleviated arthritis score, anti-CII total IgG, IgG1, IgG2a, TNF-α, IL-1β, -6, and -17, and VEGF serum levels following CIA in rats. Besides that, berberine strikingly decreased the expression of VEGF and CD34, as well as p-ERK, p-p38, and p-JNK activation in the synovium [52].

In glucocorticoid-induced osteoporosis in rats, berberine remarkably elevated bone mineral density, trabecular number and thickness, rate of mineral apposition, and bone formation rate/trabecular bone surface. Furthermore, berberine notably alleviated the trabecular separation and osteoclast/ trabecular bone surface in osteoporosis rats. They supported that berberine ameliorated osteoporosis in rats by preventing bone resorption and propagating bone formation [53].

Taken together, berberine ameliorated RA through antiinammatory and immunomodulatory properties (Fig.4).

288

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V. BaradaranRahimi and V. R. Askari

Fig. 4 The anti-arthritis mechanisms of Berberis vulgaris and its main active component, berberine. JNK c-Jun N-terminal kinase, IL interleukin, TNF-α tumor necrosis factor-α, IFN-γ interferon-gamma, TGF-β1 transforming growth factor-β1, STAT3 signal transducer and activator

9 Withania somnifera

Withania somnifera (W. somnifera), commonly named Ashwagandha, is a woody shrub belonging to Solanaceae. Its roots have been widespreadly administered in traditional Indian medicine for over 3000years. Additionally, multiple pharmacological properties have been found for W. som- nifera, namely anti-inammatory, anti-oxidant, immunomodulatory, neuro-protective, as well as anti-arthritis effects [112, 113].

9.1 Animal Studies

In CIA in rats, aqueous extract of roots of W. somnifera nota- bly reduced arthritic index, rheumatoid factor, anti-collagen type II, and CRP levels. W. somnifera also mitigated oxida- tive stress by decreasing MDA and glutathione-S-transferase activity (GST) while increasing GSH and ferric ability of plasma in CIA rats [54]. Similarly, aqueous extract or roots of W. somnifera markedly diminished clinical severity, histo- logical score, TNF-α, IL-1β, IL-6, NF-kB, MMP-8, and iNOS while elevating IL-10 levels in CIA in rats [55].

of transcription 3, AMPK AMP-activated protein kinase, iNOS inducible nitric oxide synthase, Arg-1 arginase-1, VEGF vascular endothelial growth factor

Additionally, W. somnifera root powder considerably allevi- ated paw thickness, ankle size, arthritic score, and pain, as well as radiological score in CIA in rats [114].

In CFA-induced arthritis, 70% ethanolic extract of W. somnifera roots meaningfully alleviated paw swelling, arthritic score, ESR, CRP, and rheumatoid factor in rats. It also suppressed inammation by decreasing IL-1β, -6, and -17a, TNF-α, and RANKL expression while enhancing IL-4, INFγ, and osteoprotegerin. Furthermore, W. somnifera prevented oxidative stress by decreasing MDA while improving CAT and SOD activities in CFA-induced arthritis in rats [56].

9.2 Clinical Studies

Ramakanth etal. showed that Aqueous extract of W. somnifera roots and leaves signicantly diminished modied

WOMAC score, knee swelling index, VAS pain score, stiffness, and disability in patients with knee osteoarthritis. Additionally, the extract was well tolerated, and no severe adverse effects were noticed [83]. Additionally, the chondroprotective impacts of aqueous extracts of W. somnifera root were reported in patients with osteoarthritis [115].

Role ofHerbal Medicines fortheTreatment ofArthritis

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289

10 Eucommia ulmoides

Eucommia ulmoides (E. ulmoides), commonly named Du Zhong in Chinese, is a small tree member of Eucommiaceae. Chiey, it is native to China, and its bark, leaves, seed, and male owers are widely administrated in traditional Chinese medicine. Additionally, E. ulmoides possessed multiple pharmacological activities, including anti-oxidant, antiinammatory, anti-allergic, anti-diabetes, anti-aging, cardioprotective, as well as anti-arthritis [116, 117].

10.1 Animal Studies

In CIA in rats, E. ulmoides extract markedly decreased paw volume, arthritis index, pathological score, Th17-positive cell numbers, inammatory markers (TNF-α, IL-1β, and -17), as well as RANKL mRNA levels while enhancing IL-10 and OPG mRNA level in the joint tissue [57]. Similarly, the E. ulmoides extract notably decreased ankle swelling, TNF-α, IL-1β, and IL-17 levels, RANKL/OPG ratio, MMP- 9, p65 NF-κB, and p-IKKαβexpression in CIA in rats [58]. In addition, E. ulmoides bark, leaf, and male ower extract considerably mitigated paw volume, ankle joint score, and levels of TNF-α, IL-6, -17, and -1β, and NO [59].

In the knee osteoarthritis model, E. ulmoides extract remarkably alleviated histopathological damages, and MMP1, -3, and -13 levels in the rat synovial uid and serum [60].

10.2 Clinical Studies

E. ulmoides granules signicantly diminished WOMAC pain, stiffness, dysfunction score, bone-GLA protein (BGP), recombinant human S100 calcium-binding protein, IL-17, and sphingosine 1-phosphate levels in patients with osteoarthritis and osteonecrosis [84].

Acknowledgments This study was supported by the research council of Mashhad University of Medical Sciences.

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