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Ghosal, S., et al, "Mast Cell Protecting Effects of Shilajit and Its Constituents," Phytotherapy Research, 3 (6): 249-252, 1989.

Albino rats were sensitized to horse serum every day for 14 days. The test group was given processed shilajit. On the fourteenth day, the subjects were tested for mast cell degranulation. When mast cells degranulate, they release histamine, which causes inflammation, resulting in the characteristic runny nose and watery eyes of allergic reactions. The shilajit-treated subjects' mast cells had significantly less degranulation. Less histamine was released, and fewer allergic symptoms resulted. There were also no perceptible toxic effects with dosages ranging from 100 mg/kg to 500 mg/kg, equivalent to approximately 68 grams for a 150-pound person.

Goel, R.K., et al, "Anti-ulcerogenic and Anti-inflammatory Studies With Shilajit," Journal of Ethnopharmacology, 29: 95-103, 1990.

Albino rats were given injections of potassium carrageenan to induce inflammation in their hind paws. The paws were measured for fluid volume before and, at timed intervals, after injection. Shilajit, at a dose of 50 mg/kg, reduced chemically induced inflammation by 77 percent.

Ghosal, S., et al, "Interaction of Shilajit With Biogenic Free Radicals," Department of Pharmaceutics, Banaras Hindu University, Varanasi-221005, India

Processed shilajit was tested for its ability to neutralize sulfite anion (SO), hydroxyl (HO), and nitric oxide (NO) free radicals. Chemical polymerization by free radicals was measured with and without processed shilajit. It provided almost complete protection of methyl methacrylate (MMA) against HO-radical-induced polymerization and significantly inhibited the polymerization of MMA by the SO free radicals. Processed shilajit efficiently trapped NO free radicals. The antioxidant effects were concentration-dependent. Higher concentrations of processed shilajit provided greater free-radical protection.

Ghosal, S., et al, "Antioxidant Defense by Native and Processed Shilajit - A Comparative Study," Indian Journal of Chemistry, 35B: 127-132, 1996.

The antioxidant potential of processed shilajit was compared to unprocessed shilajit and vitamin C (ascorbic acid). Peak levels of shilajit occurred 12 to 15 hours after ingestion and took more than 72 hours to metabolize. Processed shilajit showed significant antioxidant activity. It also exhibited the ability to regenerate ascorbic acid after it neutralized free radicals. The dihydroxybenzo-alpha-pyrones in shilajit recycled ascorbic acid. Unprocessed shilajit did not consistently exhibit antioxidant activity.

Bhattacharya, S.K., et al, "Shilajit Attenuates Streptozotocin-Induced Diabetes Mellitus and Decreases Pancreatic Islet Superoxide Dismutase Activity in Rats," Neuropharmacology Laboratory, Department of Pharmacology, Institute of Medical Science, Banaras Hindu University, Varanasi-221005, India

Diabetes mellitus was experimentally induced in albino rats by the administration of streptozotocin. The disease resulted in an increase of superoxide free radicals and free-radical damage to the pancreas. From the fourteenth day on, there was significant hyperglycemia, or high blood sugar, due to a lack of insulin. The test groups were given 50 mg/kg or 100 mg/kg. The shilajit had no effect on normal blood sugar levels. It stopped the progression of hyperglycemia with statistically significant changes among the 100 mg/kg group. There was also a decrease in superoxide-free-radical damage owing to the antioxidant effects of shilajit.

Bhattacharyya, Sauryya. et al. “Shilajit Dibenzo-a-Pyrones: Mitochondria Targeted Antioxidants.” Pharmacologyonline 2: 690-698 (2009).

The decrease in efficiency of mitochondria in generating energy currency (ATP) in animals and in humans is associated with aging (geriatric problems) and oxidative stress. This deficiency has a link with the systemic deficiencies of coenzyme Q10 (CoQ10) concentration and of two of its endogenous functional associates, namely, 3-hydroxydibenzo-a-pyrone (3- OH-DBP) and 3,8- dihydroxydibenzo-a-pyrone [3,8-(OH)2-DBP]. Mitochondrial targeting of the two DBPs, isolated from shilajit (the supervitalizer of Ayurveda), and of CoQ10 could be formidable strategies to augment antioxidant defense and energy generating elements for restoring normal functions of mitochondria. DBPs, as also their fatty-acyl and amino-acyl conjugates, occur in animal mitochondria and in blood where they act in tandem with CoQ10 in the electron transport chain. Administration of CoQ10 alone, in mitochondrial deficiency states, therefore, could not restore normal mitochondrial functions. The concomitant targeting of DBPs and CoQ10 to mitochondria would augment energy (ATP) synthesis and protect redox states of CoQ10 from oxidative degradation. The present findings adduce evidence of augmentation of the concentrations of DBPs and CoQ10 in mitochondria when administered, from exogenous sources, through intra-peritoneal/oral route. Their probable mechanism of action would involve the three redox states of DBPs (reduced form, semiquinone radical and quinone form) and similar redox states of CoQ10 as a measure to restore normal energy synthesizing ability of mitochondria.

Ghosal, S., et al, "The Need for Formulation of Shilajit by Its Isolated Active Constants," Phytotherapy Research, 5: 211-216, 1991.

Unprocessed shilajit samples collected from India, Nepal, Pakistan, and the Soviet Union were compared to a processed shilajit extract for their respective antistress and central nervous system effects. The processed shilajit extract produced consistently better results than the unprocessed shilajit. Stress was induced by forced swimming immobility on albino rats for six minutes. The treated rats recovered more quickly than the nontreated rats, with the processed shilajit producing the best results. Albino rats given shilajit extract resisted aspirin-induced ulcers significantly better than the control group, which received no shilajit, and the group that was fed unprocessed shilajit. The therapeutic properties of shilajit vary by region. To provide a consistent level of active ingredients, processing and standardization is necessary.

Ghosal, S., et al, "Shilajit-Induced Morphometric and Functional Changes in Mouse Peritoneal Macrophages," Department of Pharmaceutics, Banaras Hindu University, Varanasi-221005, India

Mice were given either a shilajit extract or a placebo. Their white blood cell activity was monitored prior to and, at intervals, after receiving the shilajit extract or placebo. The shilajit extract increased white blood cell activity, which rose in accordance with the dosage and the time that elasped after exposure.

Ghosal, S., "Chemistry of Shilajit, an Immunomodulatory Ayurvedic Rasayan," Pure and Applied Chemistry, 62 (7): 1285-1288, 1990.

The low-molecular-weight oxygenated dibenzo-alpha-pyrones and triterpenic acid (humic and fulvic acids) are the major active ingredients of shilajit. They affect the endocrine, autonomic, and central nervous systems, bringing about an immunomodulating result by increasing the activity of macrophages.

Bhatineharyn, S.K., "Effect of Shilajit on Rat Brain Monoamines," Department of Pharmacology, Institute of Medical Sciences, Banaras Hindu University, Varanasi-221005, India Ghosal, S., Department of Pharmaceutics, Institute of Technology, Banaras Hindu University, Varanasi-2210052, India

Male albino rats were divided into four groups:
  • Control
  • Shilajit extract (50mg/kg) one hour prior to evaluation
  • Shilajit extract (25mg/kg) daily five hours before evaluation
  • Shilajit extract (50mg/kg) daily five hours before evaluation
Neurotransmitter, serotonin, dopamine, and noradrenaline levels were measured and compared to the control group. The rats in the fourth group exhibited neurotransmitter changes associated with increased humoral, or immune, system response compared with that of the other groups. The rats in the third group experienced some improvement in neurotransmitter activity, but it was not as significant as the fourth group's.

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Bhattacharyya, Sauryya. et al. “Beneficial Effect of Processed Shilajit on Swimming Exercise Induced Impaired Energy Status of Mice.” Pharmacologyonline 1: 817-825 (2009).

Oral supplementation of a processed shilajit formulation significantly improved physiological energy status in albino mice in a model of forced swimming test (FST). There was a significant fall of adenosine tri phosphate (ATP) concentration in muscle by 82%, in brain by 33% and in blood by 35% in exercised control animals on the 7th day of a 7-day swimming regime. Post exercise shilajit treatment retrieved loss of the energy currency (ATP) in different tissues/cells in mice. The fall of ATP was attenuated to 65% in muscle, 22% in brain and 14% in blood on the 7th day of similar exercise, when the animals were treated orally with shilajit (30 mg/Kg body weight, p.o.) for the last 4 days of the swimming regime. About 18% rise in the inosine mono phosphate (IMP) concentration, a marker for energy depletion in muscle, was observed in the exercised control animals. This rise of IMP was only 5% on oral administration of shilajit. Improved status of some energy related indices, such as Adenylate Energy Charge (AEC) and Total Adenine Nucleotide (TAN), was also observed following shilajit treatment. The energy augmenting effects of shilajit were at par with those of coenzyme Q10 (CoQ10), administered orally to the animals as a positive control (15 mg/Kg body weight, p.o. x 4 days). A synergistic effect in the improvement of the energy related parameters was observed when the animals were treated with a combination of shilajit (15 mg/Kg body weight, p.o. x 4 days) and CoQ10 (7.5 mg/Kg body weight, p.o. x 4 days). Yet another improvement of shilajit treatment constituted of the CoQ status in muscle and blood of the treated animals. The FST-induced impairment of CoQ status in mice was manifested by a fall of CoQ concentration by 75% in blood and a rise in CoQ by 68% in muscle in exercised control animals on the 7th day of the swimming regime. The fall in CoQ concentration in blood was attenuated to 50% and its rise was arrested in muscle, when the animals were treated orally with shilajit (30 mg/Kg body weight, p.o. x 4 days). Effect of shilajit on blood and muscle CoQ status was at par with those of orally administered CoQ10 (15 mg/Kg body weight x 4 days).

Ghosal, S., et al, "Effects of Shilajit and Its Active Constituents on Learning and Memory in Rats," Pharmaceutical Chemistry Research Laboratory, Department of Pharmaceutics, Institute of Technology, Banaras Hindu University, Varanasi-221005, India

Lab rats were given processed shilajit, raw shilajit, or fulvic acid (derived from shilajit). The rats were then tested in a maze and a mild electric-shock-avoidance environment. The rats that were fed the processed shilajit learned to evade electric shocks more quickly and took less time to learn the maze than the control subjects did.

Goel, R.K., "Anti-ulcerogenic and Anti-inflammatory Studies With Shilajit," Journal of Ethnopharmacology, 29: 95-103, 1990.

Albino rats and male guinea pigs were given aspirin to induce gastric ulcers. The subjects that were fed shilajit had fewer incidences of ulcers. When the gastric juices were analyzed, researchers found a significant increase in the carbohydrate-protein ratio, which indicates a rise in protective mucosal secretions. The subjects that consumed shilajit were protected from ulcers owing to a jump in the secretion of the stomach's protective mucous.

Ghosal, S., et al, "Anti-ulcerogenic Activity of Fulvic Acids and 4-methoxy-6-carbmethoxybiphenyl Isolated From Shilajit," Phytotherapy Research, 2 (4): 187-191, 1988.

Two organic compounds, fulvic acid (FA) and 4-methoxy-6-carbmethoxybiphenyl (MCB), were extracted from shilajit for their ability to protect against ulcers. A single administration of the extracts did not offer protection from ulcer formation. Five consecutive days of administration of FA and MCB significantly reduced the stress-ulcer index compared with that of the control group.