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Article: Boswellia Serrata | Anti Inflammatory Supplements | Inflammation

Boswellia Serrata | Anti Inflammatory Supplements | Inflammation

Role of Boswellia serrata- as an anti-inflammatory 


Dr. Veena Deo Manager – Research and Development, Shree Baidyanath Ayurved Bhavan,Nagpur.

Miss. Sushma R. Charpe M pharm. (Pharmacology) Nagpur.

Vernacular Names:
San - Sallaki
Hindi - Salai

A medium-sized deciduous tree.

Throughout central and northern India on dry hills. The tree is common at the foot of the western Himalayas, in Rajasthan, Gujarat, Maharashtra, Madhya Pradesh, Bihar, Orissa, and Andhra Pradesh.

Parts Used:
In India, gum resin has been used in the management of several inflammatory conditions and as a topical inflammatory agent. For inflammatory conditions, a dosage of 300-400mg of standardized extract (containing 60% Boswellic acid) three times a day is suggested. Boswellia has anti-inflammatory and antiarthritic properties, which can reduce inflammation as well as pain in the body.

NSAID - Pathway of Inflammation:
There are two pathways of inflammation: cyclooxygenase and lipoxygenase. The mechanism of NSAID action is through the inhibition of prostaglandin H synthase and cyclooxygenase (COX) enzymes. Arachidonic acid, derived from membrane phospholipids, is metabolized to produce prostaglandins and leukotrienes by the COX and 5-lipoxygenase pathways respectively. There are two isoforms of COX, encoded by different genes. COX-1 is constitutively expressed and fulfils a 'housekeeping' function in the gastric mucosa, platelets, and kidneys. The COX-2 enzyme is largely induced at sites of inflammation, producing prostaglandins that cause local pain and inflammation, but COX-2 is also upregulated in the CNS, where it plays a role in the central mediation of pain and fever. Traditionally, NSAIDs such as Ibuprofen, Diclofenac, and Naproxen inhibit both COX enzymes, whereas newer NSAIDs such as Celecoxib and Etoricoxib selectively inhibit COX-2. NSAIDs have anti-inflammatory activity.

Side Effects of NSAID:
NSAID has gastrointestinal and cardiorenal side effects. Traditionally, NSAIDs can damage the gastric mucosal barrier and are an important etiological factor in up to 30% of gastric ulcers. They also reduce the integrity of the duodenal mucosa but are probably responsible for only a small proportion of duodenal ulcers. They greatly increase the risk of bleeding or perforation from preexisting gastric and duodenal ulcers. The risks of gastrointestinal events with NSAIDs are appreciable. 

Approximately 1% of patients with RA or OA are hospitalized each year because of NSAID-associated gastroduodenal bleeding. Endoscopic evidence of peptic ulceration is found in 20% of NSAID users, even in the absence of symptoms. Chronic NSAID therapy has also been associated with an increased risk of cardiovascular disease. The mechanism is incompletely understood but may involve an increased risk of thrombosis due to the inhibition of COX-2 in the endothelium. Other side effects include fluid retention and renal impairment due to the inhibition of renal prostaglandin production, non-ulcer-associated dyspepsia, abdominal pain, altered bowel habits, and rashes. Interstitial nephritis, asthma, and anaphylaxis can also occur but are rare.

  1. R. College, B. R. Walker, S. H. Ralston Davidson's, Principle and Practice of Medicine, 21st edition, Page No. 1076-1077.
  2. D. Tripathi, Essentials of Medical Pharmacology, 7th edition, Page No. 182-183. 

Boswellia Serrata - Pathway of Inflammation:

Constitution of Resin:
The resin of Boswellia serrata has been used in medicines since ancient times. Resin contains monoterpenes, diterpenes, triterpenes, tetracyclic triterpenic acid, i.e., B-boswellic acid, acetyl-B-boswellic acid, 11-keto-B-boswellic acid & acetyl-11-keto-B-boswellic acid responsible for the inhibition of pro-inflammatory enzymes.

Acetyl-11-keto-B-boswellic acid mentioned above acts as a potent inhibitor of 5-lipo-oxygenase, an enzyme responsible for inflammation. Researchers showed that acetyl-11-keto-boswellic acid & 11-keto-boswellic acid were effective in respect to aspirin at the same dose. Boswellic acid inhibits the lipoxygenase pathway.

Studies show that Boswellic acid present in resin prevents the formation of leukotrienes in the body. Leukotrienes have been identified as a cause of inflammation. Acetyl-11-keto-B-boswellic acid (AKBA) is thought to be the most powerful of the four Boswellic acids.


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Shao Y, Ho CT, Chin CK, et al. Inhibitory activity of Boswellia acids from Boswellia serrata against human leukaemia HL-60 cells in culture. Planta Med 1998; 64:328-331.

Huang MT, Badmaev V, Ding Y, et al. Anti-tumour and anti-carcinogenic activities of triterpenoid, beta-boswellic acid. Biofactors 2000; 13:225-230.

Lee KH, Spencer MR. studies of mechanism of action of salicylates. Effect of Salicylic acid on enzymes involved in mycopolysaccharides synthesis. J. Pharm Sci 1969; 58; 464-468.

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Brandt KD, Palmoski MJ. Effect of Salicylates & other nonsteroidal anti-inflammatory drugs on articular cartilage. AmJ. Med. 1984; 77; 65-69.

Structures of the Terpenes with their Activity:

Comparison of Boswellic acid with NSAID concerning Side Effects:
As mentioned, acetyl-11-keto-B-boswellic acid acts as a potent inhibitor of 5-lipo-oxygenase, an enzyme responsible for inflammation. 5-lipoxygenase produces inflammatory leukotrienes, due to which inflammation occurs, giving rise to free radical damage, cell adhesion, and migration of inflamed body areas. NSAID drugs also treat inflammation but have side effects, such as disrupting glycosaminoglycan synthesis and accelerating articular damage in arthritic conditions. NSAIDs have side effects of gastrointestinal and cardiorenal damage.

Studies show that Boswellia significantly reduced the degradation of glycosaminoglycans.


Reddy GK, Chandrakasan G, Dhar SC. Studies on the metabolism of glycosaminoglycans under the influence of new herbal anti-inflammatory agents. Biochem Pharmacol 1989; 38:3527-3534.