This page covers EGCG IV Therapy including its benefits. IV League provides mobile IV therapy for EGCG.
Certain bioactive components found in botanicals may have positive health effects. Antioxidant qualities, present in many herbal medications, are crucial in their therapeutic use. Antioxidants are substances that shield cells from free radical damage (ROS). The imbalance between antioxidants and reactive oxygen species (ROS) occurs when ROS-generating processes are activated in excess, releasing pathological levels of ROS. Numerous diseases, including cancer, have been related to oxidative stress.
Cancer is a huge global health concern. Cancer is the leading cause of death in the United States. Surgery, radiation therapy, and chemotherapy are all examples of conventional techniques used in the clinical management of cancer. Alternative management may be necessary to increase therapeutic success rates and patient satisfaction due to the complexity of human cancer. Natural products and chemotherapeutic drugs may be used together to suppress tumor growth in cancer chemoprevention or treatment.
One of the most widely consumed drinks in the world is green tea, which is rich in healthy antioxidants. Polyphenols, like phenolic acids and catechins, make up the bulk of green tea’s antioxidant components. Catechins, found in green tea, are flavonoids and are effective antioxidants and free iron scavengers. Flavonoids are a class of plant chemicals that have been shown to have powerful antioxidant effects on the cardiovascular system. It is believed that the antioxidant properties of green tea are responsible for its cancer-preventing effects.
EGCG is a catechin, a chemical found in plants that is more commonly known by its former name, epigallocatechin gallate. Catechins may be subclassified under polyphenols, another class of plant chemicals. EGCG and related catechins function as powerful antioxidants, which may provide protection from free radical-induced damage to cells. When present in excess, the highly reactive particles known as free radicals can cause damage to your cells. Consuming foods rich in antioxidants, such as catechins, may protect cells from unchecked free radical damage.
Catechins like EGCG have shown promise in preventing chronic diseases like heart disease, diabetes, and some malignancies, and reducing inflammation in the body. EGCG can be found in a variety of plant-based meals and is also commercially accessible as an extract in the form of a dietary supplement.
For the most part, EGCG has gained its notoriety as the primary bioactive component in green tea as discussed earlier. To be more specific, EGCG is widely thought to be responsible for many of green tea’s purported health advantages. Even though green tea is the most common source of EGCG, it is also present in other foods, such as
- Fruits: strawberries, cranberries, blackberries, cherries, kiwis, pears, apples, peaches, and avocados
- Tea: white, green, black and oolong teas
- Nuts: pistachios, pecans and hazelnuts
It has been suggested that EGCG can help in the prevention and treatment of chronic diseases, the reduction of inflammation, and the promotion of weight loss. Supplemental EGCG has on rare occasions been linked to significant adverse effects. If you are interested in adding EGCG to your diet, it’s best to check with your doctor first to make sure it’s safe for you to do so.
Benefits Of EGCG IV Therapy
Recently, EGCG’s various health benefits have been documented, including protection against cancer, heart disease, and neurological disorders, all of which have been linked to free radicals and reactive oxygen species.
Catechins’ antioxidant capabilities are only the beginning; they’ve also been linked to anti-diabetic, anti-bacterial, anti-inflammatory, and anti-obesity effects.
Strengthening the Heart
Green tea’s EGCG has shown promise in lowering cardiovascular risk factors like blood pressure, cholesterol, and arterial plaque buildup, according to studies.
Green tea extract with 250 milligrammes of EGCG per day reduced LDL (bad) cholesterol by 4.5 percent in an 8-week study including 33 participants. Those who took 379 milligrammes of green tea extract daily for three months saw significant improvements in their blood pressure, cholesterol, and inflammatory indicators, according to a separate trial involving 56 participants.
Although these findings are promising, more study is required to determine whether or not EGCG in green tea can actually lessen the risk of cardiovascular disease.
Boosting Brain Functioning
Green tea’s EGCG has shown promise in boosting neurological cell function and warding against degenerative brain illnesses, according to preliminary study. In certain trials, EGCG injections greatly decreased inflammation, as well as healing and regeneration of neural cells in animals with spinal cord injury.
Additional human observational studies have discovered a protective effect of green tea against cognitive decline with age, as well as against the onset of Alzheimer’s and Parkinson’s diseases. However, the existing data is conflicting. Furthermore, it is still not known if EGCG or some other chemical component of green tea is responsible for these effects.
Whether or not EGCG can effectively prevent or treat degenerative brain illnesses in humans requires more research.
Anti-inflammatory and Antioxidant Properties
The ability of EGCG to act as a powerful antioxidant and lower stress and inflammation is a major selling point for this compound. Cell damage can be caused by free radicals, which are extremely reactive particles. Oxidative stress results when there is an abundance of free radicals in the body. Cells are protected from oxidative stress damage thanks to EGCG’s antioxidant properties, and the action of pro-inflammatory molecules like tumor necrosis factor-alpha (TNF-alpha) is dampened as a result.
Cancer, diabetes, and heart disease are just some of the chronic conditions that have been linked to stress and inflammation. Accordingly, EGCG’s anti-inflammatory and antioxidant activities are believed to be among the primary reasons for its extensive disease-preventive applications.
Losing Weight
So when combined with the caffeine present in green tea, EGCG may be even more effective at helping you shed pounds. Some long-term observational studies found that drinking roughly 2 cups (14.7 ounces or 434 ml) of green tea per day was connected with decreased body fat and weight, while the outcomes of these studies were mixed.
The combination of EGCG (100-460 milligrams) and caffeine (80-300 milligrams) for at least 12 weeks has been associated to significant weight loss and reduction of body fat, according to additional human research. However, when EGCG is administered without caffeine, no significant changes in weight or body composition are detected.
History of EGCG IV
A survey of the available research in 2006, over 8000 citations were discovered that discuss the bioactivity, chemistry, production, and possible health advantages of green tea. Over four thousands of these references are specifically about EGCG and other natural components that can be found in green tea.
Green tea is made from the dried fresh leaves of the plant Camellia sinensis L. Ktze (Theaceae). The primary polyphenolic component of green tea is the natural substance known as (–)-epigallocatechin-3-gallate (EGCG, 16). Green tea also contains trace amounts of a number of additional polyphenolic chemicals that are collectively referred to as catechins.
Other types of catechins include (+)-catechin, (–)-epicatechin-3-gallate (ECG), (–)-epigallocatechin (EGC), and (–)-epicatechin (EC). More than half of the mass of this catechin combination is made up of EGCG, and a significant body of evidence indicates that EGCG (and other catechins) is accountable for the majority of the possible health advantages that are associated with the consumption of green tea.
Studies conducted on animals suggest that drinking green tea and products made with green tea that contain high concentrations of EGCG and other catechins may have a massive effect on the reduction of the risk of developing various types of cancer as well as cardiovascular disease and other medical conditions.
During this time, a significant amount of conjecture was generated in an effort to “fit” the results of in vitro studies that demonstrate the activities of EGCG on the majority of the molecular targets as well as the tumor cell cytotoxic effects exerted by EGCG and GTE at concentrations that are significantly higher than the range that is physiologically relevant.
This apparent disparity spawned a number of different hypotheses to consider as possible solutions. It has been hypothesized that the impacts of EGCG coupled with other catechins might have a synergistic effect to a greater degree than was previously believed.
Many of the advantages, side effects, and/or toxicity of high-dose or mega-dose GTE and EGCG therapy may be related to the effects seen with micromolar concentrations of EGCG, according to studies.
Similarly, the tumor cell-specific cytotoxic effects generated by elevated micromolar concentrations of EGCG might not represent phenomena that are functionally important to dietary green tea consumption but might be evident of implications that may be accomplished with increased supplementation of EGCG as well as other catechins.
Therefore, IV EGCG was developed to fight various diseases.
What Are The Mechanisms of Action for EGCG IV?
There are several mechanisms of action for IV EGCG depending upon the type of disease it is dealing with. Below are the mechanisms explained for Parkinson’s disease (PD) and Cancer, respectively:
Ferroptosis (PD) – Recent research has suggested that EGCG may be able to regulate ferroptosis, which is a regulated cell death pathway that is iron-dependent and involves a potentially lethal accumulation of lipid peroxides. Ferroptosis is caused by a combination of iron toxicity, LPO, and damaged plasma membranes. It has been demonstrated by Reddy and colleagues that EGCG has the ability to impact brain iron homeostasis in 6-OHDA-induced N27 cells. EGCG pretreatment prevented 6-OHDA from inducing an increase in the levels of divalent metal transporter-1 (DMT1) and hepcidin, as well as a decrease in the development of the iron-export protein ferroportin 1 (Fpn1), which resulted in a 28% reduction in Fe2+ uptake. Pretreatment with EGCG inhibited the stimulation of caspase-3 activity that was produced by 6-OHDA. This finding demonstrates that EGCG reduces the neurotoxicity induced by 6-OHDA through modulating iron homeostasis. This observation was supported by the findings of other studies, which demonstrated that EGCG upregulated Fpn1 in the SN and decreased oxidative stress, thereby exhibiting a neuroprotective effect against MPTP-induced neurotoxicity in mice. This observation was corroborated by the findings of other studies. On the other hand, the research conducted in 2013 showed that EGCG was able to raise the intracellular levels of GSH in a PD model. Recent findings suggested that EGCG was able to inhibit the production of rotenone-induced lipid peroxidation (LPO), which lent credence to earlier findings suggesting that EGCG treatment offered protection and prevention against PQ-induced increases in LPO and neurodegeneration in dj-1—knockdown Drosophila melanogaster.
Human esophageal Cancer – Green tea’s primary polyphenol, called (-)-epigallocatechin-3-gallate (EGCG), has been demonstrated to prevent the proliferation of a variety of cancer cell lines and to inhibit the phosphorylation of epidermal growth factor receptor (EGFR). It was found that EGCG had the same effects on esophageal squamous cell carcinoma KYSE 150 cells and epidermoid squamous cell carcinoma A431 cells. The level of phosphorylated EGFR was reduced by 32-85% when KYSE 150 cells were pretreated with EGCG at a concentration of 20 micromol/L for 0.5 to 24 hours in HAM’s F12 and RPMI 1640 mixed medium at 37 degrees Celsius prior to the addition of EGF. This treatment was performed before the addition of EGF. Extended treatment with EGCG (for either 8 or 24 hours) also resulted in a reduced level of EGFR protein (both by 80%). In esophageal adenocarcinoma OE19 cells, treatment with EGCG for 24 hours generated lower signals of HER-2/neu, which was another beneficial effect. Superoxide dismutase (SOD, 5 units/mL), or SOD plus catalase (30 units/mL), was added to the media of the cell culture in order to avoid or reduce the effects of EGCG. These enzymes were added at a concentration of 5 units/mL. In the A431 cells, an EGFR deactivation process very similar to the one described above was found. EGCG was unstable under the culture conditions for KYSE 150 cells, with a half-life of roughly 30 minutes; the formation of EGCG dimers and other oxidative products occurred. Because SOD was present in the culture medium, EGCG was able to become more stable. Additionally, its half-life was extended to be greater than 24 hours, and some EGCG was epimerized into (+)-gallocatechin-3-gallate. A mechanism for the production of H2O2 and dimerization of EGCG that is mediated by superoxide radicals has been proposed. The activity of EGCG in suppressing the growth of KYSE 150 cells was boosted as a result of the presence of SOD in the culture media, which served to stabilize EGCG. Based on the findings, it appears that under the conditions of cell culture, the auto-oxidation of EGCG results in the inactivation of EGFR, while other processes are responsible for the cell’s lack of growth. It is not yet clear whether or if the identified auto-oxidation of EGCG takes place in vivo; this is something that has to be investigated further. It is probable that SOD will be included in subsequent investigations of EGCG and other polyphenolic chemicals in cell culture in order to stabilize EGCG and eliminate the possibility of artefacts.
How Is IV EGCG Used To Treat Diabetes?
The major pathophysiological hallmark of Metabolic Syndrome (MS), and a major risk factor for cardiovascular disease and diabetes, is insulin resistance. Despite having a normal insulin levels, the peripheral target tissues (such adipose, muscle, and liver) do not respond normally to insulin. Overproduction of insulin, elevated blood sugar levels, and type 2 diabetes result when the body is unable to overcome insulin resistance. Normally sensitive tissues may overexpress insulin action if hyperinsulinemia prevents them from doing so. The increased production of endothelin-1 (ET-1), which promotes vasoconstriction, oxidative stress, cell-growth, and mitogenesis, and the activation of the vascular tissue renin-angiotensin system mediate the effects of insulin under these circumstances (RAS).
Several research have looked at EGCG’s effect on blood glucose regulation because it has been proposed as a medicinal agent for the treatment of diabetes. An improved glucose tolerance and an increase in glucose-stimulated insulin secretion were found in young db/db mice fed a diet enriched with EGCG, with islet structure being preserved in comparison to control mice. Anti-inflammatory actions may have been amplified by this flavonoid, which could account for its positive benefits. A considerable rise of anti-inflammatory cytokine IL-10 has been found to explain the delayed onset of type 1 diabetes in female non-obese diabetic mice treated with 0.05% EGCG in drinking water. RINm5F cells were subjected to recombinant IL-1beta, TNF-alpha, and IFN-gamma for 24 hours with or without EGCG pretreatment, confirming the hypothesis of the original in vitro investigation. Through lowering mitochondrial reactive-oxygen species generation and mitochondrial membrane potential and cytochrome c release, EGCG pretreatment protected -cells against inflammation-induced death.
Comorbidities associated with diabetes have been studied alongside EGCG’s effects on hyperglycemia. Thus, diabetic Wistar rat retinas and Müller cells in the retina have been studied to determine the flavonoid’s positive effects. This research showed that EGCG protected the retina from the damaging effects of hyperglycemia through an antioxidant mechanism. One of the most severe outcomes of diabetes mellitus is diabetic nephropathy. In the diabetic kidney, glucose stimulates pathways that lead to increased oxidative stress, polyol production, and advanced glycation end-products (AGE) buildup. Oral administration of EGCG for 50 days decreased hyperglycemia, proteinuria, and lipid peroxidation in a rat model study in which diabetes was generated by subtotal nephrectomy and streptozotocin injection. Other than that, it lowered the accumulation of renal advanced glycation end products, the expression of related proteins in the kidney cortex, and the prevalence of associated clinical diseases. The most prevalent consequence of diabetes, diabetic neuropathy is caused by an increase in oxidative stress, and EGCG’s qualities have recently been studied. Treatment with EGCG for 10 weeks reversed the rise of 8-hydroxy-2′-deoxyguanosine, a marker of oxidative stress and neuronal hypersensitivity, in streptozotocin-induced diabetic rats. These results point to unique features of EGCG in the treatment of diabetic neuropathy.
Osteopontin plays a pivotal function among the several mediators implicated in diabetic complications. Renal tubular and glomerular epithelial cells contain osteopontin, a profibrotic adhesion molecule. Osteopontin has been observed in renal damage due to inflammatory glomerulonephritis, obstructive uropathy, and tubulointerstitial disease, despite claims that it aids recovery from acute tubular injury. These data suggest that osteopontin can be used as a predictive marker for diabetic nephropathy. Recent research on mice with streptozotocin-induced diabetic nephropathy suggested that EGCG at 100 mg/kg might provide effective protection against diabetic nephropathy by osteopontin suppression, suggesting that this flavonoid might provide supportive aid for management of diabetes mellitus patients with nephropathy.
Understanding the benefits of EGCG against type 2 diabetes is extremely important, especially given the recent rise in the prevalence of obesity. Studies on non-obese type 2 diabetes Goto-Kakizaki rats have shown that therapy with EGCG improves glucose tolerance and glucose homeostasis in GK rats, while also decreasing oxidative stress and mitochondrial dysfunction in skeletal muscle. These improvements can be explained by a decrease in oxidative stress, a reduction in ROS production, and a prevention of mitochondrial loss and malfunction. Recently, the processes and direct effects of EGCG on glucose and lipid metabolism in HepG2 cells have been explored. A dose-dependent increase in glycogen synthesis and an inhibition of lipogenesis via increased expression of phosphorylated AMP-activated protein kinase and acetyl-CoA carboxylase have both been attributed to EGCG. Conversely, it has been hypothesized that EGCG ameliorates the insulin signaling blockage and modulates glucose uptake and production in HepG2 treated with high glucose, hence preventing or postponing a potential hepatic dysfunction. These latter observations can be explained by the fact that
- High glucose causes a drop in both the tyrosine-phosphorylated and total levels of insulin receptor, insulin receptor substrate (IRS)-1 and -2, and
- High glucose also causes a drop in both AMPK and PI3K activity, and a corresponding drop in GLUT-2 levels.
Increasing evidence suggests that the cell surface receptor, which is toll-like receptor 4 (TLR4), is crucial in the development of chronic inflammatory illnesses such as obesity-related insulin resistance. TLR4 is a natural immunological and pattern recognition receptor found in most tissues of the body. Recent research on rats, fed with a high-fat diet, found that EGCG significantly reduced free fatty acids, fasting insulin, the homeostasis model assessment-insulin resistance index and the epididymal fat coefficient, while increasing the rate of glucose infusion compared to the control group. Results also showed that insulin signaling in adipose tissues was enhanced by EGCG, which decreased inflammation by lowering macrophage concentration and disrupting the toll-like receptor 4 mediated inflammatory response pathway.
How Is EGCG IV Used To Treat Dyslipidemia?
The lipid disturbance known as dyslipidemia is defined by a rise in triglyceride (TG) levels, a rise in lipoproteins encompassing apolipoprotein B (apoB), an increase in low-density lipoprotein (LDL) particle size, and a decrease in high-density lipoprotein (HDL) cholesterol. A decrease in HDL-cholesterol and a rise in plasma LDL and TG characterize the dyslipidemia typical of MS.
The connection between EGCG and blood lipoprotein has been the subject of numerous investigations. Several of them came to the conclusion that EGCG can lower blood triglycerides, LDL-cholesterol, and total cholesterol. DNA microarray investigation on EGCG-treated HepG2 hepatocytes showed an increase in ldlr mRNA expression and a drop in extracellular apoB levels, indicating that EGCG has the potential to enhance cholesterol metabolism.
Regular tea drinkers (n = 224) were found to have lower plasma PCSK9 and low density lipoprotein cholesterol (LDL-C) levels than non-drinkers (n = 224, p 0.05) in an age- and gender-matched case control observation. In rats fed with a high-fat diet (HFD), treatment of EGCG significantly reduced circulating PCSK9 concentration and liver PCSK9 expression, and also up-regulated LDL receptor (LDLR) expression while reducing LDL-C levels. This effect of EGCG on LDLR and PCSK9 expression was also observed in a study of hepatic cells. Transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) and its results revealed that hepatocyte nuclear factor-1 (HNF-1) and forkhead box class O (FoxO) 3a were implicated in the inhibitory activity of EGCG on PCSK9 expression.
Up-regulated LDLR expression and LDL absorption in hepatocytes are the direct results of EGCG’s ability to decrease PCSK9 synthesis. This is evidenced by the fact that EGCG increases nuclear FoxO3a while simultaneously decreasing nuclear HNF1. This results in an inhibition of PCSK9 levels in both the liver and the circulation, which ultimately leads to a reduction in LDL-C levels.
How Is EGCG IV Used To Treat Hypertension?
It has been demonstrated that the compound known as epigallocatechin gallate (EGCG) can lower blood pressure. However, there has not been a lot of study done on the role that epigallocatechin gallate (EGCG) plays in enhancing vascular function in hypertensive people through the modification of endothelial nitric oxide synthase (eNOS). Oral gavage administration of EGCG at a dose of 50 mg/kg per day was administered to hypertensive mice that had been treated with Angiotensin II and were 8–10 weeks old. Every three days, the arterial systolic blood pressure (SBP) was determined by employing the tail-cuff technique of measurement. At the conclusion of the treatment, wire myographs were used to investigate the vascular reactivity of the aortae that had been isolated. Assay kits were used to detect the levels of nitric oxide (NO), cyclic guanosine monophosphate (cGMP), and tetrahydrobiopterine (BH4), while Western blotting was used to determine the presence of proteins (NOS, p-eNOS, and NOx-2).
In angiotensin II-infused hypertensive mice, in vivo treatment with EGCG for 14 days markedly reduced the upsurge in SBP, ameliorated the vascular dysfunction, enhanced the expression of p-eNOS, increased the vascular cGMP and BH4 level, and lowered the elevated ROS level and NOx-2 protein. This treatment also increased the expression of vascular cGMP and BH4 level. Overall, administration of EGCG to hypertensive mice produces a lowering effect on blood pressure. This effect can be partially attributed to an improvement in the function of the blood vessels, which is in turn suggested a connection to the ability of EGCG to reduce oxidative stress in the vascular tissue of the aorta, which in turn leads to a reduction in eNOS uncoupling and an increase in NO bioavailability.
In addition, in order to gain a better understanding of the structure-activity relationship that is responsible for the increased production of NO, a recent study investigated the effect that selective replacement of hydroxyl functions on either the B or D ring had on the EGCG-induced phosphorylation of AKT and eNOS, establishment of ROS and NO in cultured coronary artery endothelial cells, and endothelium-dependent stress relief of coronary artery rings. This research was conducted in order It is interesting to note that it has been discovered that the hydroxyl group located at the 3′ position of the gallate ring is essential, as well as, to a certain extent, located at positions 3′ and 4′ the two hydroxyl groups, for the PI3-kinase/AKT-dependent phosphorylation of endothelial NO synthase, which then leads to the subsequent NO-mediated vascular relaxation.
Intravenous IV EGCG vs. Oral Supplementation
If you are interested in adding EGCG to your diet, it is best to check with your doctor first to make sure it is safe for you to do so.
Intravenous: EGCG is administered intravenously to slow or halt the progression of cancer. Green tea has been demonstrated to suppress metastasis and prevent recurrence of cancer after therapy, as well as delay the onset of cancer itself. Researchers also found that EGCG and green tea extract could halt the progression of human cancer cell lines.
Oral: When used in supplement form, scientists recommend no more than 338 milligrammes of EGCG per day.
Molecular Structure of EGCG IV
They are constituted by a 2-phenylchromane skeleton substituted in 3, 5, 7, 3′ and 4′ position with hydroxyl groups. If the biosynthetic B-ring is derived from the gallic acid synthon, then the catechin will have a hydroxyl group substituted for the 5′ position during the biosynthesis, earning it the label “gallo” catechin. The 3′-hydroxyl group of catechin can also be esterified with gallic acid to generate “gallate,” another type of catechin. To sum up, we refer to the dextrorotatory (2s, 3r) compounds as “catechins,” whereas the levorotatory (2r, 3r) compounds are called “epi” catechins. Therefore, these eight permutations allow us to discriminate between eight distinct molecular configurations.
Its Molecular formula: C22H18O11, molecular weight is 458.40 and CAS registry number: 989-51-5.
Note: Due to research still ongoing on many aspects of the given topic, it became very difficult to take adequate information from single source or multiple sources for this document. Many topics are covered by studying the researches to deduce information due to unavailability of confirmed data.
