Pharmaceutical composition comprising an aqueous extract of...

Drug – bio-affecting and body treating compositions – Antigen – epitope – or other immunospecific immunoeffector – Conjugate or complex

Reexamination Certificate

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Reexamination Certificate

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06193977

ABSTRACT:

BACKGROUND OF THE INVENTION
1. Field of the Invention
The present invention relates generally to a pharmaceutical composition comprising aqueous extracts of Anemarrhena Rhizoma, a member of the family Liliaceae, and Phellodendron Bark, a member of the family Lilium for analgesic and anti-inflammation, and its preparing method. More particularly, it relates to a pharmaceutical composition comprising mixed aqueous extracts of Anemarrhena Rhizoma and Phellodendron Bark for analgesic and anti-inflammation against chronic gastritis, arthralgia, benign prostate hyperplasia, chronic and recurrent cystitis, cervical disc, degenerative joint arthritis, rheumatoid arthritis, tennis elbow, osteoportotic pain, migraine, diabetic neuropathy pain, Rt. flank pain, etc.
2. Description of the Related Art
There are two types of pain, one of which is fast pain sensed immediately in response to stimulants and the other is slow pain sensed gradually. The slow pain results from injuries to both the skin and the internal tissue and lasts long, while the fast pain results from injuries to the skin rather than to the internal tissue. The pain is sensed through receptors distributed over the skin and tissue, especially, those for mechanical, thermal and chemical stimulants. Upon receipt of stimulation, the receptors transmit sensation to the central nerve system. Examples of the chemicals exciting the chemical type of pain receptors include bradykinin, potassium ions, acids, proteolytic enzymes, etc. Compared to the other types of sensation, the lasting pain becomes more sensitive to stimulants and develops intolerance even to a weak stimulant.
In the body system, neurons of the brain and the vertebral column secrete those substances such as morphine that elicit an analgesic effect, and regulate the pain. Examples of the analgesic substances include endorphin, enkephalin and dynorphin secreted from the brain, and serotonin and enkephalin from the vertebral column.
The existing analgesics may be classified into two categories: (a) narcotic analgesics, e.g., codeine and dihydrocodeine and (b) non-steroidal anti-inflammatory drugs (NSAIDSs), e.g., aspirin, ibuprofen and indomethacin.
The narcotic analgesics excite receptors of the central nerve system to alleviate both light and severe pains. The narcotic analgesics are used in an increased dose depending on the degree of a pain and very effective in pain relief. However, the effect of the narcotic analgesics is practically dose-dependent and results in resistance to analgesics. In the worst cases, the narcotic analgesics adversely produce a side effect of depressing the respiratory and circulatory organs.
The NSAIDS inhibits the production of prostaglandin from arachidonic acid. Thus NSAIDS not only acts to alleviate pain and platelet agglutination attendant upon particular degenerative diseases but also reduces inflammation. The NSAIDS is to some extent effective as an analgesic and anti-inflammatory agent but often leads to side effects, i.e., stomach ulcer and bleeding of digestive organs.
Recently, there is an attempt to implement a therapeutic method that involves administration of a combination of narcotic analgesics and NSAIDs in order to maximize the beneficial effects of the above-mentioned single components while avoiding the side effects thereof.
Meanwhile, inflammation refers to a response to an tissue injury caused by pathogenic microorganisms, trauma, chemicals and heat in view of restoring the injured tissue, that is, the whole local tissue response to an injury involving secretion of several mediators from the injured tissue, induction of immunocytes and recovery of the injured tissue. This process can be summarized as follows. With tissue cells damaged or destroyed, acids and chemical mediators are released. The mediators cause the dilation of blood capillaries and increase their permeability. Histamine secreted from mast cells or basophiles initiates the response of blood vessels, and serum kinin produced from alpha-2-globulin of blood serum mediates the long-acting response of blood vessels through the blood coagulation mechanism. The blood capillary dilation increases the blood flow, and causes heat and redness. The increased permeability of the blood capillaries cause blood cells, proteins and fluids to exude into surrounding tissues, leading to swelling. Such exudation can accelerate further destruction of cells, and the increased blood pressure stimulates peripheral nerves to cause pain. The pain increases due to secretion of kinin and acids. Other mediators secreted from the tissue include serotonin, prostaglandin, reactants of the complement system, and lymphokine secreted from T-cells.
As fluid exudes from the capillaries, leukocytes (i.e., neutrophils and monocytes) migrate to the damaged region and digest or dissolve inflammation-causing substances to recover the damaged area. Another important cells in the inflammatory reaction are monocyte-originated macrophages that also participate in phagocytosis and rapidly proliferate when the tissue is damaged. Fusion of the macrophages or amitotic division of large fragments produces giant cells.
The inflammatory reaction occurs locally or entirely in the body system. In some cases, pyrogens secreted from bacteria stimulate the thermoregulatory center in the brain and produce a fever which, in turn, raises metabolic rate, decreases appetite and results to depletion of somatic tissue with muscle and body fat. Fluid losses may result in dehydration. Lymph fluid absorbs fluid and the protein exuded from the blood capillaries, and transports them to the lymphnode, which causes lymphadenitis characterized by lymphnode enlargement and pain.
As described, inflammation is a primary mechanism of the body system to repair tissue damage or protect against latent infection. However, an untimely or chronic inflammation reaction can result in pain or diability.
There can be used two types of antiinflammatory medications, the one of which involves inhibiting production and exudation of inflammatory cells and the other involves reducing secretion of inflammation mediators. The currently used medical agents may be divided into NSAIDs, capable of producing both analgesic and inflammatory effects as described above, and steroidal anti-inflammatory drugs. The NSAIDs are widely spread as analgesic and inflammatory agents and have a mechanism of inhibiting production of prostaglandin from arachidonic acid. Corticosteroids used against inflammation not only inhibit generation of prostaglandin but also act on beta-adrenergic receptors of leukocytes to inhibit secretion of inter-leukins (ILs) and reduce permeability of the blood vessels, which in turn inhibits exudation of blood and inflammatory cells. Despite the therapeutic effects, corticosteroids have been reported to produce a number of side effects, such as increasing the size of erythrocytes, weight gain, accelerating progression of osteoporosis and weakening blood capillary, raising blood pressure and stomach ulcer. Cromolyn sodium is also used as an inflammatory agent involving stabilization of the cytoplasmic membrane of mast cells and inhibiting activation of macrophages, but produce a number of side effects.
The following description deals with two cases of benign prostate hyperplasia and chronic cystitis in detail.
Benign prostate hyperplasia(BPH) is one of the prevailing diseases among at least 50% of aged males over fifty and estimated as a degenerative disease involving the enlargement of prostate gland due to intact androgen supply as the man gets old. In the early stage of forties, nodules can generate in the transition(grandula) and periurethral zones (stromal). The nodules formed in the transition zone continuously grow into the major part of the main mass of the BPH, in which case the central and peripheral zones are compressed and fibromuscular tissue develops between the BPH tissue. This progresses over several years and symptoms appear as the enlarged prostate obstructs the urinary track.
The symptoms of benign prostate hyperplasia ca

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