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A REVIEW ON HERBAL DRUGS WITH POTENTIAL ANTI-ARTHRITIC ACTIVITY

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A REVIEW ON HERBAL DRUGS WITH POTENTIAL ANTI-ARTHRITIC ACTIVITY

Shanaz Banu and Leemol Varghese *

Dayananda Sagar University, Bengaluru, Karnataka, India.

ABSTRACT: Rheumatoid arthritis (RA) is a general inflammatory disorder touching about 1.3% of the grown-up census of the world. Over the last two decades, a significant development has been done in the thoughtfulness of RA pathophysiology, best outcomes, and successful treatment strategy, and the credit of the significance of diagnostic agents and treating RA near the beginning. Earlier than novel treatments were obtained, RA caused notable incapability and deaths. At present, it is customary that principal diagnostic agents and therapy are significant and helpful. Development in the treatment of RA made it likely to manipulate signs in inflammatory arthritis. The early hour diagnosis and treatment of RA can prevent or reduce the progression of joint erosion to about 90% of patients; by this means irreversible disability can be prevented. In advance and more effective treatment significantly improves the prognosis of RA. The advancement of novel instruments to assess disease activity and recognize remission has brought about innovative treatment strategies to inhibit RA ahead of joint damage forever. The pharmacological therapy consists of the nonsteroidal anti-inflammatory drug (NSAIDs), glucocorticoids (GC); disease-modifying antirheumatic drugs (DMARDs), biological drugs is of two types: 1) Monoclonal antibodies, 2) bisphosphonate agents. The price of a few treatments is considerable, but their use has come down with the advancement of biosimilars. A target-treatment strategy aims to decrease disease activity by around 50% in three months and achieve a reduction of disease succession in six months, with continuous therapy if needed, which can prevent RA-related disability. There is a restoration of attention in plant products because of the present belief that green medicine is safer and more trustworthy than expensive synthetic drugs. The outlook is towards the synchronized multidimensional research intended to correlate botanical and phytochemical activities to exact anti-arthritic activity is achieved.

Keywords: Rheumatoid arthritis, Phytoconstituents, Early Diagnosis, Drug treatment

INTRODUCTION: RA is an inflammatory rheumatic disorder in which moving articular and extra-articular parts cause ache, disability, and death 1, 4. It causes chronic inflammation, which is a systemic autoimmune disorder, at first disturbing to small bones and then the larger ones, eventually to skin, eyes, heart, kidneys, and lungs.

Frequently, joints and cartilage of bones are damaged; tendons and ligaments are destroyed 5, 7. Constant inflammation causes erosion of joints and practical injury in the huge bulk of patients 8, 11.

RA results in severe ache, bulge, rigidity, and lack of activity in bones. It damages any bone still commonly affects bones of the wrist and fingers. Further, women are affected than men by RA. It usually begins in middle age and is very general in elderly people 12, 15. Natural products from plants play an extraordinary function in treating and prevent many pathological conditions from olden times. Research examined by World Health Organization (WHO) has concluded that approximately 80% of world’s population depends on conventional therapy 16, 21. In the USA, about 121 therapeutic agents are prescribed, 90 of them are from the natural agents chiefly from plants in a straight or indirect way. Herbal remedy will be a source to alleviate signs of RA and handle the problems linked with current therapy of allopathic agents 27.

Signs: RA signs depend on the extent of membrane inflammatory reaction. During membrane inflammation, disease is vigorous. AS membrane inflammatory reaction suppresses, the disorder becomes dormant, as called remission. During the active state, RA symptoms appear: exhaustion, lack of energy, decreased craving for food, low fever, muscle and ache, flush, bump, softness, deformity, nodules, rigidity, and lack of movement reduced bone activity 22, 23.

As reported by the Centres for Disease Control and Prevention (CDC), the signs typically distress equivalent bones on either side of body 24, 28.

Rarely, RA damages the joint, resulting in the contraction of voice cords to change the tone of voice. This causes horse voice 29, 31. Signs are usually on and off. Through remission, symptoms vanish, or can be mild. Conversely, through a flare, symptoms will be severe 32.

FIG. 1: SIGNS OF RA

Pathophysiology: The core reason of RA is unidentified. Although viruses, bacteria, and fungi have extensively been assumed, but not been proved. It is thought that the propensity to grow RA may be hereditary 33, 34. RA is classified as an autoimmune disease, which occurs due to the over-activity of the immune structure by offending the body's own cells and tissues. In people with RA, the immune system stimulates unusual inflammation in the membrane that covers joints i.e., the synovial membrane. Inflammation of synovium; causes ache, swelling, and stiffness of joints. In harsh situations, inflammatory reactions damage the bone, joints and surrounding tissues within the joints, resulting in bigger damages 35. Immune cells, called lymphocytes, are stimulated, and chemical messengers (cytokines, such as tumor necrosis factor/TNF, interleukin-1/IL-1, and interleukin-6/IL-6) are produced in the inflamed regions 36, 39. Synovial fibroblasts are major players in RA. They motivate a pro-inflammatory situation in the synovial membrane, cooperate with the immune system, and control the differentiation of monocytes to osteoclasts 39, 42.

Major genetic agents of RA are variations in Human Leukocyte Antigen (HLA), particularly the HLA-DRB1 gene. The amino acids synthesized by HLA assist the immunity to differentiate its own amino acids apart from foreign ones of viruses and bacteria 43, 48.

Environmental agents also appear to take a prime role in causing RA. Smoking tobacco, contact with silica, and long-term periodontal disorders raise the threat of budding RA. Studies regarding gut organisms that can stimulate the beginning of RA in hereditarily vulnerable candidates 49, 50.

FIG. 2: RHEUMATOID ARTHRITIS PATHOPHYSILOGY CD40=cluster of differentiation 40, co-stimulatory protein present of antigen presenting cell(APC); CD40L= cluster of differentiation 41-LIgant present of th cell, bind to CD40 to activate APC; TCR=T cell receptor; BCR=B cell receptor MHC= major histocompactibility complex= surface receptor, with its ligand activate TCR; FCR receptor = protein receptor present on immune cells, CCR=c-c-motif receptor= beta chemokine receptor; CCL5= chemokine (c-c-motif) ligant-5=RANTES= its chemo tactic for neotrophils; CCL2= chemokine (c-c-motif) ligant-2= MCP; CCL3= chemokine (c-c-motif) ligant-3MIP-1; CXCL8=IL8; LTB=TNF-C= induce inflammatory response; VEGF= vascular endothelial growth factor, Pannus= abnormal fibrovasculor  tissue lies over joint surface; MM matrix metalloproteinase PGE= prostaglandin E; IL-IB= interleukin -1 beta; cathepsin k= enzyme regulating bone remodelling; ROS= reactive oxygen species; NO= nitric oxide; IL-4= interleukin-4; IL-10 = interleukin-10 IL-13= interleukin-13; T cell = T lymphocyte; B cell = B lymphocyte; TNF= tumor necrosis factored; IL-1= interleukin-1 

Risk Factors and Complications: CDC reported that patients with an elevated threat of attacking RA can comprise individuals of age 60 years or above, female, overweight, smoking 50, 55.

Diagnosis: The diagnosis depends on the clinical presentation. The existence of rheumatoid factor and citrulline antibody (Abs). The occurrence of nodules and X-ray changes 55.

Antinuclear Antibody (ANA) Test: Presence of antinuclear Abs in blood. The test detects antinuclear Abs in blood and confirms autoimmune disease. On taking the blood samples from veins of arms, positive result on an ANA test explains that antinuclear antibodies were confirmed in blood. Individuals may expect a positive result if:

  • Person has SLE (lupus).
  • Person has an autoimmune disorder.
  • Person has a viral infection.

Cyclic Citrullinated Peptide Antibody: This test helps confirm RA and differentiate it from other arthritis and estimate the prognosis of RA patients. Cyclic citrullinated peptide antibodies are those released by the immune systems which are focussed against cyclic citrullinated peptides (CCP). This test identifies and calculates anti-CCP antibodies in the blood. Citrulline is formed in the body due to the metabolism of amino acid arginine. Though, in joints with RA, this translation happens at a higher rate. Citrulline modifies protein configuration and stimulates an immune response, forming autoantibodies in opposition to joint proteins. The CCP antibody test confirms the diagnosis of RA and is used in recognizing patients with the quickly erosive type of disease.

Erythrocyte Sedimentation Rate (ESR): ESR is a test that calculates how rapidly RBC settles down. In general, red cells settle comparatively slowly. A faster rate confirms inflammation in the body. Higher ESR shows inflammatory disorders 55, 59.

Stages Of Rheumatoid Arthritis” The stages of RA by the condition of cartilage, ligament, and joints are as follows.

Stage I: early RA: Negative effect on X-ray, whereas symptoms of joint thinning may be present.

Stage II: moderate progressive: X-ray confirmation of joint thinning surrounding a bone with or devoid of little joint erosion.

  • little cartilage destruction is probable
  • Joint movement is restricted; the absence of bone deformities are seen
  • Atrophy of surrounding soft tissue
  • Damage of muscle adjacent to joints.

Stage III: severe progression:

  • X-ray examination of joints shows erosion
  • Joints deformities with reversible stiffness joints
  • Widespread soft tissue atrophy

Stage IV: terminal progression:

  • X-ray observation of joint damage and osteoporosis surrounding the joints.
  • Joint deformities with irreversible stiffness of the joints (ankylosis)
  • Widespread soft tissue atrophy and abnormalities

Physicians Categorize The Position RA Patients as Follows:

  • Capable of carrying out normal functions of everyday
  • Capable of carrying out common self-care except in working outdoor like playing sports.
  • Capable of executing normal self-care but restricted in other jobs
  • Incomplete capability to execute normal self-care and activities 60, 63.

Treatment:

Non-Pharmacological Treatment:

Rest: During a flare, the patient should rest. Swollen and acheful bones make signs worse.

Exercise: Upon remission, signs are gentle; patients must often exercise to improve health and reinforce the soft tissues surrounding the bones. The finest workout is that which does no tension on the bones, like swimming.

Diet: Subsequently, healthy food with lots of fruits and vegetables will improve the patient, allow feeling better, and maintaining a healthy weight 64, 65.

Pharmacological Treatment:

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): Chronic administration and high concentrations result in adverse effects like gastric upset, elevated BP, kidney damage, and liver injuries 66.

Corticosteroids: They intend to decrease aches and inflammatory responses and can slow down bone injuries, although they may not heal RA. Corticosteroids are very useful in acute signs or short-term flares. Chronic therapy of corticosteroids causes severe side effects like being overweight 67.

Disease-modifying Antirheumatic Drugs (DMARDs): DMARDs decrease the succession of RA and stop irreversible erosion of the joints and other soft tissues by intrusive overactivity of the immune system. It is largely successful in the near beginning stages. Adverse effects liver includes marrow and immune suppression.

Tumour Necrotic Factor Alpha Inhibitors (TNF-Alpha Inhibitors): TNF-alpha is an inflammation-causing agent. TNF-alpha blockers avoid inflammatory reactions.

Blockers diminish ache, morning rigidity, and inflamed joints 67, 68. Probable adverse effects comprise elevated threat of infection, blood-related diseases, heart failure, demyelinating disorders.

Surgery: Surgery restores injured bones, corrects deformity, and decreases ache.

Arthroplasty: It is a complete bone replacement; surgeons take out injured structures and add a metallic or plastic prosthesis 69.

Tendon Renovate: If tendons have loosened or ruptured surrounding joints, surgery helps renovate them 70.

Synovectomy: This process involves the elimination of the synovial membrane due to inflammation and ache.

Arthrodesis: The doctor can combine bones to reduce ache and to steady joints.

FIG. 3: TREATMENT OF RHEUMATOID ARTHRITIS

Herbal Therapy: Numerous anti-arthritic agents have been developed and used in RA treatment; still, these agents experience many adverse effects resulting in limited efficacy.

The herbal therapy approach now has a wide variety, usually not seen with artificial agents. Green medicine has been extensively studied as harmonizing and optional agent since the olden days in the alleviation of inflammation and immune system diseases.

The present pharmacotherapeutics administered by conservative formulations give healing profits merely till suboptimal level; therefore take up all the problems in the RA therapy. Green phytoconstituents for RA therapy are given as follows in Table 1.

TABLE 1: HERBAL THERAPY FOR RA 71

S. no. Natural product Source Part used Active principal MOA and molecular pathways involved Challenge and adverse effect
1 Boswellia Serrate Indian frankincense salai/ salaigu gglu The resin of Boswellia Oleo gum resin from the trunk of the tree Triterpenic acid that is b- Boswellic acid acety b- Boswellic acid 11 keto b-Boswellic acid and acetyl 1-keto-b- b- Boswellic acid Acts via 5-LOX inhibition Stomach pain, nausea diarrhoea and allergic rashes reported
2 Turmeric Curcumin Curcuma L

onga

 Curcuma Longa Linn Dried as well as fresh rhizome Curcumin It acts by inhibition of COX, 5-LOX and glutathione S-transferase Higher dose long term administration causes nausea and diarrhea
3 Gamma limol  (GLA) Rapeseed canola oil soy beans walnuts and flex seed linseed oil Plant seed oil O-mega 6 fatty acids Dietary GLA it converted directly to DGLA increased levels of DGLA promote the synthesis of in- flammattory metabolites i.e, series prostaglandins PGEI suppress chronic inflammation It is safe at the dose 2.8  g/day up to year besides it causes softening of tools belching and intestinal gas to
4 Ginger Zingiberofficin

ale

 Zingiberofficinails Linn Rhizomes It contains high proportions sesquiterpenes, predominantly zingiberene and gingerols It inhibits PG and LTs biosynthesis via an inhibitory action on PG synthetase and 5-LOX, and addition to this also inhibits pro-inflammatory cytokines such as IL 1 TNF, and IL-8 It is safe, but some minor side effects such as heartburn diarrhoea, stomach discomfort, and skin irritation may take place
5 Thunder God vine Tripteryguimwifordii Skinned root (extract) Its major compositions
are di-terpenoid triptolide		 It interferes with the production of PGs cytotoxic T-cell proliferation and IL-2 too GIT disturbances such as nausea, abdominal pain, indigestion flatulence, constipation, hair loss male infertility, and significant immune suppression
6 Celastrol Tripteryguimwil for dii (lei gong teng thunder of god vine), which belongs to the Celastraceae family Root and work A yellow quinoidenor triterpene called Celastrol which is a pentacyclic  triterpene Celastrol has beneficial antiaarthritic effects by suppersion of pro-inflammatory cytokines mediated MMP-9 expression and lipopolysachardies Diarrhoea headache nausea, and infertility, especially at high dose
7 Thymoquinone (TQ) TQ is obtained from the volatile oil of black the black caraway seed Nigella sativa Ranuunculaaceae family Volatile oil of the black seed TQ is a major bioactive it constituent of the volatile oil og black seed (54%) It extracts antiarrhritic action against carrageenan induced paw oedema in rats by inhiniting the inflammatory mediators It is safe and may cause allergic rashes
8 Sinomenine It is obtained from the root of Sinomenine Actum Roots Sinomenine is alkaoid Sinomenine may inhibit proliferation of synovial fibroblasts in arthritis It produces abnormal immunosuppression
9 Paeoniflorin It is obtained from the root of a Paeonia Roots It is a major constituent of paeonialacflora It extracts anti-arthritic action by inhibition of IL-6 and COX-2 Abdiminal upset and skin Rashes
10 Asiatocide and madecesso side Two whole plants of cebtellaasiatica whole pant It contains large amounts of pentacyclic triterpenoid, including asiatico and madecassoside It provides production against joint destruction in CIA mice Skin allergy, burring sensations, headache nausea, extreme drowsiness and contact dermatitis
11 Epigallocate chin It is obtained  from oldenlandia Diff uss and fruits zizphusjujube Fruit Epigallocatechin gallate also know as epigallocatachin 3-gaalate ia an ester of epigallocatachin and gallic acid It showed effective action against arthritis by TNF, an inhibition It hampered iron absorption in a dos-dependent
12 Naringin It is obtained  from grapes and citrus fruits Grapes and citrusfruit Naringin is a flavanone-7-O-glycoside It showed antiiarthritic action by suppression of MMP-9 Biiter and taste
13 Hesperidin It is obtained  from the fruit of citrus aurrations Citrus fruits Flavanone glycoside It suppression the T-lymphocyte proliferation and IL-2 production in rats too Limited bioavailability
14 Resveratrol It is obtained  from grapes and redn wine Grapes red wine and berries Resveratrol polyphenolic compounds It mediated antiarthritic action by targeting NF-Kb and simultaneously decreases AGEs-stimulated expression and prevent AGEs- mediated destruction of CLA Poor oral bioavailability

AA, adjuvant arthritis; AGE, advanced glycation end products; CIA, collagen-induced arthritis; COX, cyclooxygenase; DGLA, dietary gammalinolenic acid; GLA, gammalinolenic acid IL, inter-leukin; MMP-9, metalloprotieinase-9; MOA, mechanism of action, NF-KB,  nuclear factor- KB; TNF; tumour necerosis factor-a.

CONCLUSION: RA is an assorted disorder, and the response to therapy is unpredictable. DMARDs must be used almost immediately following diagnosis; methotrexate is a top early drug; illness ought to be often monitored; a combination of green medicine with synthetic drugs decreases the progression of the disease.

There is a restoration of attention in indigenous natural agents due to the prevalent faith that plant products are more harmless and reliable than expensive artificial medicines. In outlook, extra synchronized multidimensional research is required to correlate botanical and phytochemical properties to precise pharmacological activity in RA therapy. It is trusted that coming years will observe a drastic swing in how medical studies are conceived in RA.

ACKNOWLEDGEMENT: Nil

CONFLICT OF INTEREST: Authors declare no conflict of interest.

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    How to cite this article:

    Banu S and Varghese L: A review on herbal drugs with potential anti-arthritic activity. Int J Pharm Sci & Res 2021; 13(4): 1479-87. doi: 10.13040/IJPSR.0975-8232.13(4).1479-87.

    All © 2022 are reserved by International Journal of Pharmaceutical Sciences and Research. This Journal licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License.

Article Information

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1479-1487

851 KB

511

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English

IJPSR

Shanaz Banu and Leemol Varghese *

Dayananda Sagar University, Bengaluru, Karnataka, India.

leemolvarghese1@gmail.com

30 June 2021

03 August 2021

05 August 2021

10.13040/IJPSR.0975-8232.13(4).1479-87

01 April 2022

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