85 % of stroke occurrences in the western world are ischemic. That means, the stroke results from blockage of a major cerebral artery (cerebral ischemia). Cerebral ischemia is the second leading cause of death and the third leading cause of morbidity worldwide due to brain tissue death (Hankey, 2013). ‘Cerebral ischemia by reperfusion’ is a condition characterized by an initial blood flow restriction followed by the subsequent restoration of blood flow and re-oxygenation.
According to some experimental studies, it has been found that both a High Fat Diet (HFD) and genetic obesity were accompanied with increased cerebrovascular tissues, an increase in hypertension and increased infarct size (Deutsch et al, 2006).
This study reported that a high fat diet causes significantly greater loss of cortical tissue and extensive remodeling post ‘cortical contusion injury’ (CCI) than in a standard diet group.
Western medicine has only one drug approved by the FDA for use within 3 hours of ischemic stroke onset, Rt-PA. This drug however has potential side effects and so is reserved for emergent care only. This severely limits resources available for improving ischemic stroke mortality and morbidity. Other options for drug therapy are prophylactic protection, and it has been seen that in animal models of stroke with many drugs pre-treatment yields better outcome than post-stroke treatment (Jonas, 1995).
According to modern Western clinical practice guidelines, anti-platelet therapy is recommended in all patients with ischemic stroke. It reduces deep venous thrombosis and pulmonary embolism. Patients with ischemic stroke or transient ischemic attack are treated with the statin group of hypolipidemic drugs to reduce the risk of vascular outcomes.
Aspirin is the most commonly used drug in patients with coronary heart diseases. It is used as a first line treatment for transient ischemic attacks. Aspirin is prescribed immediately for patients who have sustained ischemic stroke, thus aspirin and atorvastatin were taken as reference standard drugs to be compared to the gum resin from the tree Commiphora whighitii (Guggal) in recent studies.
Guggal, an important staple of Ayurvedic medicine, has been used for thousands of years in the treatment of arthritis, inflammation, obesity, cardiac protection, anti-ulcer, anti-epileptic and disorders of lipid metabolism. Guggal is a member of the Burseraceae family and is found in arid areas of India, Bangladesh, and Pakistan. Guggulipid is an extract of resin from the tree Commiphora whighitii. Guggulipid has been marketed in India since 1988 as a hypolipidemic agent, similar to statins.
Clinical studies also support that guggulipid showed hypolipodemic effect, anti-oxidant effect and anti-inflammatory effect, likely due to inhibition of NF-kappa B activation (which is responsible for ischemia induced neuronal injury) and cardioprotective effect in ischemic patients. Preclinical studies reported that guggulipid inhibited the platelet aggregation and had anti-inflammatory effect (via inhibition of TNFα expression), delayed progression of atherosclerosis, and anti-hypercholesterolemic (Urizar & Moore, 2013).
Prophylactic drug treatment significantly reduced the potentiated nitric oxide (NO) release followed by high fat diet and middle cerebral artery occlusion. It has been demonstrated from various studies that high levels of NO production exacerbated neuronal damage. Guggulipid pretreatment showed this same neuroprotective property. It is known from various studies that ischemic stroke is evoked by inflammatory reaction and brain inflammation, produced during reperfusion, is due to the accumulation of inflammatory cells and microvascular dysfunction in damaged areas of neuronal tissue. Previous Guggulipid research has demonstrated neuroprotection due to its hypolipidemic, antioxidant, anti-inflammatory and anti-thrombotic activities.
Guggalipid does not carry the same side effects as its pharmaceutical counterparts, yet has similar efficacy as statins for reducing blood lipids. It’s as effective as aspirin for inhibiting platelet aggregation and anti-inflammation in one natural herb.
REFERENCES
Ahmad, M. A., Najmi, A. K., Mujeeb, M., & Akhtar, M. (2016). Protective Effect of Guggulipid in High Fat Diet and Middle Cerebral Artery Occlusion (MCAO) Induced Ischemic Cerebral Injury in Rats. Drug Research, 66(8), 407–414. https://doi.org/10.1055/s-0042- 107787
Deutsch C, Portik-Dobos V, Smith AD et al. Diet-induced obesity causes cerebral vessel remodeling and increases the damage caused by ischemic stroke. Microvascular Research 2009; 78: 100–106
Hankey GJ. The global and regional burden of stroke. Lancet 2013; 1: 239–240
Jonas S. Prophylactic pharmacologic neuroprotection against focal cerebral ischemia. Ann NY Acad Science 1995; 765: 21–25
Urizar NL, Moore DD. Guggulipid: a natural cholesterol-lowering agent. Ann Rev Nutr 2013; 23: 303–313, 15
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