Bacopa monniera supports the functions of the central nervous system
Mode of action of the bacosides
Anxiolytic effects of Bacopa monniera
Anti-convulsive action
Beneficial effects in the management of animal models of Alzheimer's disease

The biological effects of Bacopa monniera are well documented in traditional as well as scientific literature. The most important of these are the effects of the plant, plant extracts and isolated bacosides on cognition and memory functions, their anxiolytic effects and their role in the management of convulsive disorders.

Preclinical studies

  1. Antioxidant action :

The results of a recent study suggest that the cognition promoting functions of Bacopa monniera may be partially attributed to the antioxidant effects of the bacosides. Currently, a number of deteriorative processes in the body are attributed to the action of damaging free radicals. During the physiological process of respiration, inhaled and tissue incorporated oxygen oxidizes cellular components and biomolecules. This process results in the generation of oxidative products, free radicals and reactive oxygen species, when titled towards excessive activity by external factors  (e.g. improper nutrition) or internal factors (e.g. disease). These free radicals are highly reactive chemical molecules, which react with biological compounds causing tissue damage by a process called "free radical pathology".

The aging process exemplifies the cumulative result of deterioration of individual cells, tissues and organs caused and promoted by free radicals. The human body has built-in mechanisms to counteract free radicals. These mechanisms are collectively known as the body's antioxidant defense. Unfortunately, in most instances the antioxidant defense is gradually overwhelmed by the aging process, disease or a combination of both. The inflammatory processes associated with microbial or viral infections, the progression of cancer and neurological disorders are just a few disease conditions which contribute to depletion of the antioxidant defense system of the body. This defense system is constituted by the enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX).

Lipid peroxidation is essentially a "free radical chain reaction" involving the following stages:

  1. Initiation

Hydrogen is abstracted from a polyunsaturated fatty acid side chain by a free radical species:

  • CH+R*------- C*+RH
  • C*+O2 ---------- -CO2*
  2. Propagation

The fatty acid side chain peroxyl radical -CO2 * attacks adjacent fatty acid side chains.

  • CO2*+-CH-------- -CO2H + -C*

The propagation continues, leading to accumulation of lipid peroxides in the membranes, destabilization of the membranes and the entry of damaging ions. Peroxyl radicals attack ions as well as membrane proteins. An antioxidant terminates the propagation of free radicals either by accepting and quenching them or by retarding the "initiation" step by reducing the generation of free radicals.

One study determined the effects of alcohol and hexane extracts of Brahmi on lipid peroxidation induced by ferrous sulfate and cumene hydroperoxide in rat liver homogenate. The alcohol fraction of Bacopa monniera furnished greater protection against both inducers, ferrous sulfate and cumene peroxide . Table 4.1 indicates the effective inhibitory doses.



ED50 (mg) ferrous sulfate

ED50 (mg) cumene hydroperoxide

Alcoholic extract



Hexane extract




The results were also compared with known antioxidants, tris (2-amino-2-hydroxymethyl-1,3-propanediol) (a hydroxyl trapper), EDTA (a metal chelator) and the natural antioxidant, Vitamin E. (Note: 100 mg of the alcoholic extract of Brahmi was equivalent to 247 mg of EDTA (0.66mM) and 58 mg of Vitamin E.) Tris did not show any protective effect, while Brahmi (alcoholic extract), EDTA and Vitamin E, offered dose-dependent protection against ferrous sulfate-induced peroxidation (Fig. 4.1).


Fig. 4.1 Comparative effects of Vitamin E and Brahmi on lipid peroxidation in rat liver homogenate

The authors also observed that Brahmi only slightly protected against the oxidation of reduced glutathione at doses lower than 100 mg/ml, while higher concentrations enhanced the rate of oxidation. The authors concluded that Brahmi's mechanism of antioxidant action could be attributed to metal chelation at the initiation level of the free radical-induced, chain reaction or the quenching of free radicals at propagation level.

A more recent study explored the antioxidant activity of Bacopa monniera in the rats' frontal cortex, striatum and hippocampus. The levels of the antioxidant enzymes, SOD, CAT and GPX, were measured following the administration of a standardized extract of Bacopa monniera (bacoside A content 82± 5%, administered in doses of 5 mg/kg and 10 mg/kg orally) for 7, 14 and 21 days. These results were compared with the effects induced by (-)deprenyl (selegiline hydrochloride, a well-known neurological antioxidant, 2 mg/kg orally) for the same time period. The enzyme activities were investigated in the frontal cortex, striatum and hippocampus after 14 and 21 days.

After 14 and 21 days, Bacopa monniera extract induced a dose-related increase in SOD, CAT and GPX activities in all brain regions investigated, while (-)deprenyl induced an increase in the frontal cortex and striatum but not the hippocampus. The results suggest that Bacopa monniera extract exhibits significant antioxidant effects, and these effects extend to the hippocampus, the seat of memory and cognition, unlike deprenyl. The authors concluded that increased free radical scavenging may explain, at least in part, the cognition-facilitating action of Bacopa monniera extract documented in the ancient Ayurvedic texts and in modern scientific literature.


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