5 Amazing Health Benefits of Monkey Sugarcane

Monkey sugarcane (Costus afer) has five amazing health benefits that would surprise you. The plant, which is always greenish and perennial, is usually found in West African countries ad beers white and yellow flowers. Every part of Monkey sugarcane offers an amazing health benefits. Other common names of Costus afer include Okpete, Tete-egun, or Mbritem.

The plant contains some bioactive compounds that have nephroprotective properties on the kidneys. It also protects against neurodegenerative diseases as well as protection of the pancreatic beta cells.


Phytochemical Components of Costus afer


Monkey sugarcane leaves are usually green.

Costus afer contains several phytochemicals in their roots, stems, rhizomes and leaves. Some of the phytochemicals include:

  • Alkaloids
  • Tannins
  • Phenols
  • Saponins
  • Triterpenes
  • Glycosides

The rhizome contains steroidal saponins such as

  • Diocin
  • Paryphllin C
  • Aferoside B
  • Aferoside C

The aerial parts contain kaempferol-3-O-R-L-rhamnopyranoside while the roots contain additional Aferoside A, Aferoside B and Aferoside C.


Health benefits of Monkey Sugarcane

The health benefits of Monkey sugarcane, especially in the treatment of rheumatoid arthritis, may be attributed to its bioactive compounds such as kaempferol and Aferosides. It is used in treating a wide range of illness which include:

  1. Treatment of Ulcer

The rhizome pulp and leave extracts are used in treating ulcers when taken, mostly by oral administration. Both the leaves and rhizome extracts increase gastroprotective factors, antioxidants such as glutathione, and decreases lipid peroxidation.


  1. Treatment of Diabetes Mellitus

Diabetic patients would find the leaf and stem extracts of Monkey sugarcane useful in treating diabetes mellitus, as both extracts enhance glucose clearance and reduce hyperglycemia by increasing cellular glucose uptake.


  1. Monkey Sugarcane Possesses Antioxidant Properties

The extracts of the various parts of Costus afer, especially the leaf extract is used in treating oxidative stress. It increases the activity of plasma superoxide dismutase (SOD) and increases the levels of glutathione and serum electrolytes such as Na+ and HCO3 . Other enzymes whose activities, Costus afer extract increases include catalase and glutathione-S-transferase.


  1. Protection of The Kidneys From Toxic Damage

The plant leaves, when taken, protect the kidneys from toxic and harmful substances. It also protects the β-cells of the pancreas from alloxan-induced damage. This supports its anti-diabetic efficiency as healthy β-cells promotes insulin production and glucose transport across the inter- and intra-cellular compartments.

Read also (Monkeypox virus infection)


  1. Possesses Anti-inflammatory Activity

Costus afer contains strong anti-inflammatory components such as Kaempferol, Aferoside A and Zn2+. They exert their anti-inflammatory activities by regulation the signaling activity of NF-kB pathways. Also, they inhibit the production of IFN-ϒ and IL-2, both which are proinflammatory factors. This regulatory effect of Costus afer extracts makes them useful in the treatment of rheumatoid arthritis and other inflammatory diseases. Aside the regulatory role they play on NF-kB signaling pathways, they also exert inhibitory effect on the cyclo-oxygenase-2 (COX-2) and interfere with G-protein-mediated signal transduction.


Side Effects of Monkey sugarcane

When taken for a long period of time, the side effects from the use of Costus afer may include:

Sufficient reduction of red blood cells, which results in anemia.

Increased weight of the liver and vacuolar changes in the hepatic cells.

When taken by pregnant women, may lead to miscarriage.



G. E. Omokhua, “Medicinal and socio-cultural importance of Costus afer (Ker Grawl) in Nigeria,” African Research Review, vol. 5, no. 5, pp. 282–287, 2011.

G. N. Anyasor, O. Ogunwenmo, O. A. Oyelana, and B. E. Akpofunure, “Phytochemical constituents and antioxidant activities of aqueous and methanol stem extracts of Costus afer Ker Gawl. (Costaceae),” African Journal of Biotechnology, vol. 9, no. 31, pp. 4880–4884, 2010.

A. N. Ezejiofor, Z. N. Igweze, N. A. Udowelle, and O. E. Orisakwe, “Histopathological and biochemical assessments of Costus afer stem on alloxan-induced diabetic rats,” Journal of Basic and Clinical Physiology and Pharmacology, vol. 28, no. 4, pp. 383–391, 2017.

A. N. Ezejiofor, C. N. Orish, and O. E. Orisakwe, “Cytological and biochemical studies during the progression of alloxan-induced diabetes and possible protection of an aqueous leaf extract of Costus afer,” Chinese Journal of Natural Medicines, vol. 12, no. 10, pp. 745–752, 2014.


Effect of Black Seed Thymoquinone on Rheumatoid Arthritis

Thymoquinone (2-isoprpyl-5-methyl-1,4-benzoquinone) is the most active component of Black cumin (Nigella sativa) seed oil. It is widely used in traditional medicine to treat a wide range of illnesses.

According to various research findings, thymoquinone exert important health-beneficial effects including antioxidant, anti-inflammatory and anti-cancer effects. As an antioxidant agent, thymoquinone normalizes glutathione levels and increases the activity of antioxidant enzymes such as glutathione peroxidase, catalase, and superoxide dismutase.


Black Cumin Tea Contains Thymoquinone

Black cumin seed is made into a tea and served as an antioxidant agent. Since it contains thymoquinone and other biologically active phytochemicals, black cumin seed tea should be recommended for patients who suffer rheumatoid arthritis. It can also be served to cancer patients who are undergoing chemotherapy.

How To Prepare Black Cumin Seed Tea

  • To prepare black cumin seed tea, assemble 2 cups of water, 2 tea spoonful of raw black cumin seeds and honey. Then follow the steps as follows:
  • Add the 2 cups of water and black cumin seeds in a pot and heat till it boils.
  • Remove from heat once it boiled.
  • Cover the pot and allow it to steep for about 10 minutes.
  • Strain the water into a cup using a mesh. You may add the seed to enjoy the whole benefits if you so wish.
  • Add two spoonful of honey and stir
  • Serve and enjoy your tea


Benefits of Thymoquinone and Black Cumin Seed Tea in Treatment of Rheumatoid Arthritis

The uncontrolled inflammation associated with rheumatoid arthritis arises as a result of the uncontrolled production and activity of various inflammatory cytokines, TNFα, IL-1, IL-17, IL-6 and the resulting inflammation is responsible for the pain, tenderness, swelling, redness and stiffness of joints.

Black cumin seeds and especially thymoquinone has been shown to be beneficial against rheumatoid arthritis and autoimmune diseases.


Thymoquinone Inhibits NF-kB Signaling In Rheumatoid Arthritis

NF-kB regulates the expression of many genes, enzymes, cytokines, cell cycle regulatory molecules as well as angiogenic factors. It induces inflammation by influencing the expression several pro-inflammatory cytokines, chemokines , acute phase proteins and growth factors.

Thymoquinone inhibits NF-kB induced inflammatory response in rheumatoid arthritis patients by inhibiting its translocation into the nucleus. Thymoquinone also inhibits NF-kB activities by suppressing TNF-induced-NF-kB activation. This is done by inhibiting TNF-induced IKBα phosphorylation and degradation as well as p65 phosphorylation and nuclear translocation.


Thymoquinone Inhibits Prostaglandins and COX-2 in Rheumatoid Arthritis

Prostaglandins (PGs) are arachidonic acid metabolites. They are found at elevated levels in synovial fluid and also in synovial membrane, where they function in the development of vasodilation, fluid extravasation and pain in synovial tissues. Aside these functions, Prostaglandin E2 (PGE2) and COX are upregulated in synovial tissues in rheumatoid arthritis patients, where PGE2 synergizes with IL-23 to stimulate Th17 cell proliferation.

Th17 in turn stimulates the release of pro-inflammatory cytokines and promotes bone resorption. PGE2 also mediates complex interactions that lead to the development of articular cartilage erosions and juxta-articular bone.

Cyclooxygenase enzymes (COX), especially COX-2 are involved in inflammatory responses. COX-2 is induced by pro-inflammatory cytokines, mainly IL-1.

Thymoquinone suppresses the expression of COX-2 protein by inhibiting NF-kB signaling pathway activation and induces the expression of cytoprotective enzymes.

Effect of Thymoquinone on PI3k/Akt Signaling Pathway

Phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway is an intracellular regulatory signal transduction pathway that is activated by toxic substances or cellular stimuli that regulate many cellular processes including cell growth, survival and apoptosis.

When abnormally activated, PI3K/Akt signaling pathway is involved in the pathogenesis of many diseases including diabetes mellitus, cancer, and rheumatoid arthritis. In RA, PI3K/Akt signaling pathway play important role through the expression of different types of pro-inflammatory mediators that degrade IKβ and activate NF-kB signaling pathway.

Thymoquinone induces apoptosis by blocking PI3K/Akt signaling pathway in DU-145 cell line. It also deactivate PI3K/Akt and NF-kB signaling pathway and regulate various gene products such as p65 and COX-2.



J.K. Kundu, L. Liu, J.-W. Shin, Y.-J. Surh., Thymoquinone inhibits phorbol ester-induced activation of NF-κB and expression of COX-2, and induces expression of cytoprotective enzymes in mouse skin in vivo Biochem. Biophys. Res. Commun., 438 (4) (2013), pp. 721-727


Umar, J. Zargan, K. Umar, S. Ahmad, C.K. Katiyar, H.A. Khan Modulation of the oxidative stress and inflammatory cytokine response by thymoquinone in the collagen induced arthritis in Wistar rats Chem. Biol. Interact., 197 (1) (2012), pp. 40-46


Vaillancourt, P. Silva, Q. Shi, H. Fahmi, J.C. Fernandes, M. Benderdour

Elucidation of molecular mechanisms underlying the protective effects of thymoquinone against rheumatoid arthritis J. Cell. Biochem., 112 (1) (2011), pp. 107-117


Thymoquinone inhibits IL-1β-induced inflammation in human osteoarthritis chondrocytes by suppressing NF-κB and MAPKs signaling pathway Inflammation, 38 (6) (2015), pp. 2235-2241


Khan, A. Sureda, T. Belwal, S. Çetinkaya, İ. Süntar, S. Tejada, H.P. Devkota, H. Ullah, M. Aschner. Polyphenols in the treatment of autoimmune diseases. Autoimmun. Rev., 18 (7) (2019), pp. 647-657


Stańczyk J, Kowalski ML. Rola cyklooksygenaz oraz prostaglandyn w patogenezie reumatoidalnego zapalenia stawów [The role of cyclooxygenase and prostaglandins in the pathogenesis of rheumatoid arthritis]. Pol Merkur Lekarski. 2001 Nov;11(65):438-43.


Rheumatoid Arthritis (RA)

Rheumatoid arthritis (RA) is an autoimmune disease, which is characterized by chronic inflammation at the skeletal joints. Most times, the bone and cartilage of the joints affected are destroyed, and tendons and ligaments weakened. As the disease progresses, it eventually affects the skin, eye, heart, kidneys and lungs.

According to reports, RA affects more females than males, and is predominantly observed in the elderly. The prevalence rate of RA reported in 2002 ranged from 0.5% to 1% of the population. It also has regional variation. It primarily affects the lining of the synovial joints and can cause progressive disability, premature death, as well as socioeconomic burdens.


Symptoms of Rheumatoid Arthritis (RA)

Common symptoms of RA include:

  • Stiffness at affected joints, especially in the morning
  • Fatigue
  • Fever
  • Weight loss
  • Tender, swollen and warm joints
  • Rheumatoid nodules under the skin

Early stage of Rheumatoid arthritis tends to affect the smaller joints, particularly the joints that join the fingers to the hands and toes to the feet. As the disease progresses, the symptoms may progress to the wrists, knees, ankles, elbows, shoulders and hips.


Pathogenic Roles of Immune Cells in Rheumatoid Arthritis (RA)

As an autoimmune disorder, immune cells such as B-cells, T-cells and macrophages play important roles in RA pathogenesis. They can either reside in synovium or circulate in peripheral blood.


Roles of B-Lymphocytes in RA Pathogenesis

B-cells secrete physiologically important proteins such as rheumatoid factors (RFs), anti-citrullinated protein antibodies (ACPA) and pro-inflammatory cytokines in supporting RA.

Auto-reactive B-cells are B-cells that identify host antigens and go on to destroy such cell or tissue. Normally, auto-reactive B-cells are eliminated by repair mechanisms either at the time when it is still immature B-cells in the bone marrow, or before the B-cells become mature naïve B-cells. Both processes of repair mechanisms are highly regulated by two immune checkpoints; they are

  • The central B-cell tolerance checkpoint and,
  • The peripheral B-cell tolerance checkpoint.

The central B-cell tolerance checkpoint is controlled by B-cell growth factors that regulate B-cell receptor (BCR) and toll-like receptor (TLR) signaling. But the peripheral B-cell tolerance checkpoint involves extrinsic B-cell factors such as regulatory T-cells (Treg) and serum B-cell activating factor (BAFF).

In patients with RA, both checkpoints are defective, which leads to the larger production of auto-reactive mature naïve B-cells. Such defect is usually caused by a mutation in PTPN22 gene that disrupts the BCR signaling pathway in central B-cell tolerance checkpoint. This impairment is irreversible and cannot be treated effectively with anti-inflammatory drugs.

In impaired peripheral tolerance checkpoint, mature naïve B-cell levels are elevated. The elevated mature naïve B-cell expresses both poly-reactive and human epithelia (HEP-2) reactive antibodies in RA patients. This dysfunction in peripheral checkpoint results in defective Tregs and in B-cell resistance to suppression and apoptosis.

Also, in patients with RA, BAFF is increased in the presence of cytokines and chemokines, as well as through TLRs activation. The increased BAFF expression further prolongs the survival and maturation of auto-reactive B-cells, exacerbate autoimmune conditions.


Roles of T-Lymphocytes in RA Pathogenesis

The chronic immune response of RA is contributed by CD4+ T-cells. During activation of T-cells, CD4+T-cells interact with human leukocyte antigen (HLA) or major histocompatibility complex class II (MHC-II) molecules and also co-stimulate molecules such as CD28, that are expressed on the surface of APC. This leads to the onset of downstream PI3K signaling pathway, which leads to the maturation of CD4+ cells. Subsequently, the interaction leads to the antigenic activation of naive CD8+ T-cells, which promote inflammation.

CD4+ T-cells also associate with particular MHC-II alleles, HLA-DR4, which contains similar amino acid motifs in the third hyper-variable region of DRB-chain. This interaction then leads to a more aggressive form of RA. The systemic morbidity associated with RA such as vasculitis and acute coronary syndrome is correlated with CD4+CD28 null.

In addition to cell-to-cell interaction, CD4+ T-helper (Th) cells contribute to the pathogenesis of RA through the secretion of cytokines and chemokines, which are important immune modulators in cell-mediated immunity.

Type 1 T-helper (Th1) cells, which are highly activated in RA, secrete pro-inflammatory cytokines such as IFNϒ, IL-2, and TNF-α. Th1 cells also activate macrophages to act as an APC to present MHC-II molecules to the T-cells. Meanwhile, CD4+ Th2 cells on the other hand secrete anti-inflammatory cytokines such as IL-4 and IL-5 and play central roles in B-cell activation and in immunoglobulin (Ig) class switching to IgE. A T-cell subset, Th17 cells secrete Il-17 which stimulates production of pro-inflammatory cytokines, chemokines, and matrix metalloproteinases (MMps).


Roles of Macrophages in RA Pathogenesis

Macrophages are found in synovial tissue where most of it resides within the tissue in a resting state under normal conditions. But in an inflamed joint, they regulate the secretion of pro-inflammatory cytokines and damaging enzymes, which are associated with inflammatory responses and subsequently, joint destruction. They also mediate the recruitment of lymphocytes, cartilage damage, joint erosion, angiogenesis and fibroblast proliferation. Macrophages act as APC and are found to highly express HLA-DR and leukocyte adhesion molecules, which allow macrophages to participate in T-cell activation alongside B-cells.

The macrophage-mediated T-cell activation results in the production of effectors T-cells as well as expression of resulting pro-inflammatory mediators like IL-1α, IL-1β, and MMPs, which support RA pathogenesis.


The Role of Cytokines in RA pathogenesis

Cytokines are proteins that function as mediators in cell signaling; they comprise monokines, lymphocytes, ILs, IFNs, colony stimulating factors (CFS) and chemokines. Pro-inflammatory cytokines play pivotal roles in the pathogenesis of RA.

In early pathogenesis, the predominant cytokines that are secreted from T-cells and stroma cells are IL-13, IL-14 and IL-15. These cytokines cause the inflammatory response and contribute to chronic inflammation. In RA patients, pro-inflammatory cytokines such as TNF-α, IL-1 and IL-17 usually outweigh the protective effects of the anti-inflammatory cytokines such as IL-4, IL-11 and IL-13, which results in the cytokine-mediated inflammation.

In RA, B-cells and macrophages, which are APCs, present arthritis-associated antigens to T-cells and activate the signaling cascades to secrete cytokines. The cytokines so activated stimulate the activation of chondrocytes and osteoclasts and produce MMPs, which degrades the matrix of articular cartilage leading to bone resorption.


Role of NF-kB in RA Pathogenesis

NF-kB activation plays a pivotal role at the stage of initiation and also at the stage of perpetuation of chronic inflammation in RA. The NF-kB activation is triggered in T cells by the engagement of the T cell receptor and the CD28 receptor with their ligands, MHC-II and the co-stimulatory molecule CD80 and CD86 presented by APCs. The T cell receptor CD28 work in synergy in induction for T cells activation and proliferation, such as IL-2, IL-2 receptor (IL-2R), and IFNϒ. In turn, activated T cells elicit NF-kB activation in APCs.

The suppression of NF-kB inhibited expression of many proinflammatory molecules, including IL-1, TNFα, IL-6, IL-8, ICAM-1 and VCAM-1 but had no effect on the expression of anti-inflammatory cytokines IL-10 and IL-1 receptor antagonist. It thus suggests that NF-kB activation facilitates the impaired balance of proinflammatory and anti-inflammatory molecules in the arthritic joint.


Treatment of Rheumatoid Arthritis (RA)

There is presently no cure for rheumatoid arthritis. However, symptoms of RA can be abated when treated with disease-modifying antirheumatic drugs (DMARDs). Some of the medications for Rheumatoid Arthritis include:

Steroids. Corticosteroid medications reduce inflammation and slow joint damage.

NSAIDS. Nonsteroidal anti-inflammatory drugs (NSAIDs) reduce pain and inflammation. E.g. includes Ibuprofen and Naproxen sodium.

DMARDs. Conventional DMARDs can slow the progress of rheumatoid arthritis and prevent the joints and other tissues from permanent damage.


What is the Mechanism of Action of Corticosteroid?


Corticosteroid is synthetic drug that mimic the adrenal hormone, cortisol, used in the management of many inflammatory and autoimmune health conditions. They modify the functions of epidermal and dermal cells and of leukocytes involved in proliferative and inflammatory diseases of the skin.

Corticosteroids can be used in treating several health conditions, such as:

  • Asthma
  • Allergies
  • Eczema
  • Hives
  • Psoriasis
  • Chronic obstructive pulmonary disease
  • Gout
  • Lupus
  • Multiple sclerosis
  • Autoimmune diseases

Types of corticosteroids

Corticosteroids come in different forms. Some of the corticosteroids used in treating inflammations include cortisone, prednisone and methylprednisolone. Prednisone is the most commonly used type of steroids used in treating certain rheumatoid diseases like rheumatoid arthritis or lupus.


How to administer corticosteroid

Corticosteroid comes in different forms based on their ease of administration. They can be localized of systemic.

Localized steroids target a specific part of the body and can be applied through:

  • Eye drops
  • Ear drops
  • Skin cream and ointments
  • Inhalers

Systemic steroids circulate through the blood. They can be applied by oral, intravenous or subcutaneous injection.


Mechanism of action of Corticosteroids

In its mechanism of action, corticosteroid react with receptor proteins in the cytoplasm to form a steroid-receptor complex. The complex thus formed moves into the nucleus, where it binds to DNA. By binding to the DNA and changing the transcription of mRNA, corticosteroid stimulates the production of glycoprotein called Lipocortin. Lipocortin inhibits the activity of phospholipase A2, which releases arachidonic acid, the precusor of prostanoid and leukoctrienes, from phospholipids. Corticosteroid also inhibits the transcription of mRNA responsible for interleukine-1 formation. Thus, by inhibiting arachidonic acid metabolism and interleukin-1 formation, steroids produce anti-inflammatory, immunosuppressive and anti-mytogenic effects.

Adverse effects of corticosteroids

Corticosteroid in its mechanism of action, especially glucocorticosteroid, has been shown to stimulate osteoclastic activity in the first 6-12 months of therapy, followed by a decrease in bone formation and life span. It promotes the apoptosis of osteolasts and osteocytes. It can also cause adrenal suppression in patients that are been treated with it.  Other side effects of steroids include cushingoid appearance and weight gain, hyperglycemia and diabetes, cataracts and glaucoma.