Hicart
Hicart Uses, Dosage, Side Effects, Food Interaction and all others data.
Chondroitin sulfate is a glycosaminoglycan considered as a symptomatic slow-acting drug for osteoarthritis (SYSADOA). The SYSADOA status suggested a pain relief and increased joint mobility after a relative long regular administration, as well as a long-lasting effect after the end of the treatment. Chondroitin sulfate is composed of alternating 1,3-N-acetyl-β-d-galactosamine and 1,4-β-d-glucuronic acid units which bear 4-O- and/or 6-O-sulfations at the N-acetylgalactosamine units disposed of in specific patterns. Depending on the predominating disaccharide unit, it will present different biological activities. Chondroitin sulfate is sold as an OTC dietary supplement in North America and it is a prescription drug under the EMA in Europe.
In clinical trials, chondroitin sulfate has been reported a significant pain relief. Some reports have shown no slow in joint damage. The effects of chondroitin sulfate have been very controversial. One of the characteristics of chondroitin is a slow onset of action with a maximal effect attained after several months. Chondroitin sulfate has been reported to have anti-inflammatory properties by reducing the synovitis and prevent proinflammatory cytokine up-regulation in arthritis models.
It is also registered an anabolic effect of chondroitin sulfate in which it induces the synthesis of hyaluronate in synovial cells, it increases type II collagen and proteoglycan synthesis.
Boric acid exhibits minimal bacteriostatic and antifungal activities . Boric acid is likely to mediate antifungal actions at high concentrations over prolonged exposures .
| Trade Name | Hicart |
| Generic | Manganese Sulphate + Chondroitin Sulfate + Sodium Borate + Methylsulfonylmethane + Glucosamine Sulfate Potassium Chloride |
| Weight | 3mg |
| Type | Tablet |
| Therapeutic Class | |
| Manufacturer | D D Nutritions India |
| Available Country | India |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Chondroitin sulfate, used with glucosamine, is indicated to alleviate pain and inflammation from primary osteoarthritis. This supplement is reported to improve joint function and slow disease progression. Osteoarthritis is characterized by progressive structural and metabolic changes in joint tissues, mainly cartilage degradation, subchondral bone sclerosis and inflammation of synovial membrane.
Studies have proposed the potential use of chondroitin sulfate as a nutraceutical in dietary supplements.
No FDA- or EMA-approved therapeutic indications on its own.
Hicart is also used to associated treatment for these conditions: Arthritis, Backache, Muscle Strain, Osteoarthritis (OA), Soreness, Muscle, Sprains, Eye lubrication, Joint supplementationConjunctivitis, Stye, Ulceration of the mouth, Oral Hygiene, Irrigation of the ocular surface therapy
How Hicart works
Chondroitin sulfate functions as a major component of the intricate extracellular matrix. It is proposed that chondroitin sulfate supply can provide new building blocks for the synthesis of new matrix components.
The anti-inflammatory effect of chondroitin sulfate is thought to be caused by the inhibition of the synthesis of inflammatory intermediates such as the inhibition of nitric oxide synthase, COX-2, microsomal prostaglandin synthase 1 and prostaglandin E2. It is reported also an inhibitory activity in the toll-like receptor 4 which will later inhibit inflammatory cytokines, NFkB and MyD88. This activity suggests a modulation of the MAP kinase pathway. On the other hand, some reports have pointed out an induction on the PKC/PI3K/Akt pathway in neuroblastoma.
The anabolic effect of chondroitin sulfate is suggested to be caused by the inhibition of metalloproteinases such as MMP-1, -3 and -13 as well as ADAMTS-4 and -5.
Information regarding the mechanism of action of boric acid in mediating its antibacterial or antifungal actions is limited. Boric acid inhibits biofilm formation and hyphal transformation of Candida albicans, which are critical virulence factors . In addition, arrest of fungal growth was observed with the treatment of boric acid .
Toxicity
Chondroitin sulfate does not present a carcinogenic potential. On tolerability assays, it has been shown to present great safety and good tolerability without significant severe side effects.
The acute oral LD50 in rats is 4500-5000 mg/kg and the intradermal LD50 in rabbits is 10,000 mg/kg. Individuals are likely to be exposed to boric acid from industrial manufacturing or processing. Local tissue injury from boric acid exposure is likely due to caustic effects. Systemic effects from boric acid poisoning usually occur from multiple exposures over a period of days and involve gastrointestinal, dermal, CNS, and renal manifestations. Gastrointestinal toxicity include persistent nausea, vomiting, diarrhea, epigastric pain, hematemesis, and blue-green discoloration of the feces and vomit . Following the onset of GI symptoms, a characteristic intense generalized erythroderma follows . Management of mild to moderate toxicity should be supportive. In case of severe toxicity, dialysis may be required in addition to supportive treatment.
Volume of Distribution
After intramuscular administration of chondroitin sulfate, the apparent volume of distribution was 0.40 ml/g. When administered orally, the apparent volume of distribution changed to 0.44ml/g.
Volume of distribution ranges from 0.17 to 0.5 L/kg in humans, where large amounts of boric acid are localized in brain, liver, and kidney .
Elimination Route
Chondroitin sulfate is absorbed from the gastrointestinal tract. The absorbed portion reaches a ratio of 10% as unchanged chondroitin sulfate and 90% as depolymerized low-molecular-weight derivatives. This absorption depends on the sulfation status. The bioavailability of chondroitin sulfate ranges from 10-20% following oral administration. Reports have shown a consistent accumulation of the compound in joint tissue. The steady-state is attained after 3-4 days and it takes around 3-6 months to obtain the maximal effect.
After intramuscular administration of chondroitin sulfate, the peak plasma level of 3.8 mcg/ml was reached after 90 min. When given orally, the peak plasma concentration of 4.6 mcg/ml was reached after 240 min.
Boric acid is well absorbed from the gastrointestinal tract, open wounds, and serous cavities but displays limited absorption in intact skin . Following intraperitoneal injection in mice, the peak concentration was reached in about 1.0-1.5 hr in the brain whereas the value was 0.5 hr in other tissues .
Half Life
The approximate half-life of chondroitin sulfate and its derivative metabolites is 15 hours. After intramuscular administration of chondroitin sulfate in humans, the elimination half-life of the chondroitin sulfate was of 275 min. When administered orally, the elimination half-life was presented at 310 min.
According to human cases of poisoning, the elimination half-life of boric acid ranges from 13 to 24 hours .
Clearance
A case report of acute boric acid poisoning following oral ingestion of 21 g of boric acid presents the total body clearance of 0.99 L/h before hemodialysis .
Elimination Route
Chondroitin sulfate is excreted in the urine as intact polymers and as partial degradation products. After intramuscular administration, about 37% of the administered dose is excreted by urine during the first 24 hours as high- and low-molecular-weight derivatives.
Regardless the route of administration, boric acid predominantly undergoes rapid renal excretion of >90% of total administered dose as unchanged form. Small amounts are also excreted into sweat, saliva, and feces. Following administration as ointment, urinary excretion of boric acid accounted for only 1% of the administered dose .
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