Wosulin 30/70

Indications

• Diabetes mellitus (type 1 and type 2)
• Diabetic ketoacidosis
• Hyperglycemia due to other conditions
• Management of blood glucose levels during surgery
• Continuous subcutaneous insulin infusion therapy

Dosage

Children: For children aged 1-17 years, insulin is administered immediately before meals or when necessary shortly after meals, according to individual requirements. Specific dosing should be determined based on blood glucose monitoring and should be referred to the BNF for Children for precise guidance.

Adults: The dosage of insulin varies based on individual needs and is typically guided by blood glucose monitoring. It is recommended to consult local protocols for specific dosing instructions.

Mechanism of action

Insulin has a direct inhibitory effect on lipase, which is involved in the mobilization of fatty acids. In the absence of insulin, there is an abnormally high rate of conversion of protein to glucose, primarily in the liver. Insulin stimulates glycogen synthesis and enhances facilitated diffusion of glucose and the active transport of amino acids, although the exact mechanisms for these actions are not fully understood.

Pharmacodynamics

Insulin's primary pharmacodynamic effect is the reduction of blood glucose levels. It promotes the uptake of glucose by cells, increases glycogen synthesis in the liver, and inhibits gluconeogenesis. Insulin also influences lipid metabolism by inhibiting lipolysis and encouraging fat storage. Additionally, insulin enhances protein synthesis by promoting amino acid uptake into cells.

Pharmacokinetics

Insulin is administered by injection and is rapidly absorbed into the bloodstream. Its onset, peak, and duration of action depend on the formulation used (e.g., rapid-acting, short-acting). The half-life of insulin is typically around 5 to 10 minutes, but its effects can last several hours depending on the formulation. It is metabolized primarily in the liver and kidneys.

Contra-indications

• Hypersensitivity to insulin or any of its excipients
• Hypoglycemia

Adverse effects

• Hypoglycemia
• Injection site reactions
• Weight gain
• Allergic reactions
• Edema
• Lipodystrophy

Interactions

• Metreleptin may increase the risk of hypoglycemia when used with insulin
• Fibrates may increase the risk of hypoglycemia when used with insulin
• Macrolides may increase the risk of severe hypoglycemia when used with insulin
• Clarithromycin may increase the risk of severe hypoglycemia when used with insulin

Precautions

• Monitor blood glucose levels regularly, especially when changing insulin preparations
• Use caution in patients with renal impairment, as insulin clearance may be reduced
• Patients should be advised about the risks of hypoglycemia and how to manage it
• Should be used with caution in patients with cardiovascular disease

Pregnancy

Insulin is generally considered safe for use during pregnancy, but dosages may need to be adjusted.

Breast-feeding

Insulin is compatible with breastfeeding; insulin does not pass into breast milk in significant amounts.

Storage

Store unopened vials or pens in a refrigerator (2-8°C). Once opened, insulin can be stored at room temperature (below 25°C) for up to 28 days, depending on the formulation.

Formulations

• Insulin human 500 units/ml solution for injection
• Insulin human 100 units/ml solution for injection
• Insulin porcine 100 units/ml solution for injection

Indications

• Rectal and anal disorders
• Haemorrhoids
• Pruritus ani

Dosage

Children: Refer to the BNF for Children for appropriate dosing information.

Adults: For rectal use using aerosol spray: 1 spray up to 3 times a day for no longer than 7 days without medical advice. For ointment: apply several times daily, for short-term use only.

Mechanism of action

Phenol exerts its effects by acting as a potent proteolytic agent. At concentrations of 5% to 7%, it can dissolve tissue through proteolysis. When injected near a nerve, it produces chemical neurolysis, affecting nerve fibers nonselectively. Local anesthetic effects are typically observed within 5 to 10 minutes of application.

Pharmacodynamics

Phenol's pharmacodynamic properties include its ability to cause tissue dissolution and local anesthesia. The local anesthetic effects result from its action on the nerve fibers, leading to a temporary loss of sensation in the affected area. The proteolytic action can assist in the treatment of various skin and mucosal conditions by facilitating tissue breakdown.

Pharmacokinetics

Phenol is absorbed through mucosal surfaces when applied locally. Its metabolism involves biological oxidation and phase I functionalization, primarily through cytochrome P450 enzymes. The elimination of phenol occurs through metabolic pathways, and it can be detected in urine as a result of its metabolism.

Contra-indications

• Infection
• Known hypersensitivity to phenol or its components

Adverse effects

• Local irritation
• Burning sensation
• Paraesthesia
• Vision disorders
• Skin reactions
• Adrenal suppression

Interactions

• Caution with other local anesthetics due to potential additive effects

Precautions

• Use for short periods only-no longer than a few days
• Avoid excessive application, especially on sensitive areas
• Consult product literature for specific guidelines

Pregnancy

Data on the use of phenol during pregnancy is limited; caution is advised.

Breast-feeding

Limited information available; caution is recommended when used in breastfeeding mothers.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Ointment
• Suppository
• Aerosol spray

Indications

• Chronic pain management
• Attention deficit hyperactivity disorder (ADHD)
• Certain types of diabetes
• Hypertension
• Seizure disorders

Dosage

Children: Refer to specific product guidelines for dosing in children, as this will depend on age, weight, and condition being treated.

Adults: Refer to specific product guidelines for dosing, as this can vary widely depending on the formulation and condition being treated. Adjustment may be necessary based on individual patient factors.

Mechanism of action

Biphasic formulations typically contain both immediate-release and extended-release components. The immediate-release component acts quickly to provide rapid therapeutic effects, while the extended-release component is designed to release the active ingredient over a longer period. This dual-release mechanism allows for sustained drug levels in the bloodstream, improving efficacy and reducing the frequency of dosing.

Pharmacodynamics

The pharmacodynamics of biphasic drugs can vary based on the specific active ingredients used and their respective therapeutic actions. Generally, the immediate phase produces rapid effects, while the second phase maintains therapeutic levels, leading to prolonged action. This can help manage conditions where both quick relief and sustained control are necessary.

Pharmacokinetics

The pharmacokinetics of biphasic formulations will depend on the specific drugs involved. Typically, the absorption of the immediate-release phase occurs rapidly after administration, leading to peak plasma concentrations within a short time. The extended-release phase is designed to prolong the duration of action by controlling the release rate, which results in a slower absorption and a more gradual increase in plasma levels over time. The elimination half-life will vary depending on the characteristics of the active pharmaceutical ingredients.

Pregnancy

The safety of biphasic formulations during pregnancy has not been established. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether biphasic formulations are excreted in human milk. Exercise caution when administering to breastfeeding women.

Storage

Store at room temperature, away from moisture and heat. Keep out of reach of children.

Indications

• Electrolyte replacement
• Volume expansion in hypovolemic patients
• Management of hyponatremia
• Support in intravenous fluid therapy

Dosage

Children: Refer to the BNF for Children for appropriate dosing in paediatric patients, as dosages may vary based on the formulation and clinical condition.

Adults: Refer to specific product information or clinical guidelines for dosage recommendations, as disodium is often part of combination products.

Mechanism of action

Disodium compounds often function by providing sodium ions that are essential for various physiological processes. Sodium ions play a critical role in maintaining osmotic balance, nerve impulse transmission, and muscle contraction. In the context of intravenous solutions, disodium helps to restore electrolyte balance in patients.

Pharmacodynamics

The pharmacodynamics of disodium is primarily related to its role in electrolyte balance and fluid homeostasis. Sodium ions are vital for the function of excitable tissues, including neurons and muscle cells. Changes in sodium levels can affect blood pressure, hydration status, and overall cellular function.

Pharmacokinetics

The pharmacokinetics of disodium compounds depend on their specific formulation and route of administration. When administered intravenously, disodium is rapidly distributed in the extracellular fluid, where it helps to maintain osmotic pressure. Sodium is primarily excreted by the kidneys, and its levels can be influenced by fluid intake, dietary sodium, and renal function.

Pregnancy

Use with caution. Consult a healthcare provider for specific guidance.

Breast-feeding

Use with caution. Consult a healthcare provider for specific guidance.

Storage

Store at room temperature, away from moisture and direct sunlight.

Indications

• Constipation
• Preparation for surgical or diagnostic procedures involving the rectum
• Decreasing intraocular pressure in certain ocular conditions

Dosage

Children: For children aged 2 to 6 years, 2 g to 5 g of glycerin may be used as a suppository. Children aged 6 to 12 years may use 5 g to 10 g as needed. For specific pediatric dosing, please refer to the BNF for Children.

Adults: For rectal use, 4 g to 10 g of glycerin may be administered as a suppository as needed.

Mechanism of action

When administered rectally, glycerin draws water from the tissues into the feces due to its hygroscopic action, which reflexively stimulates bowel evacuation. Additionally, glycerin creates an osmotic gradient that leads to a decrease in intraocular pressure by facilitating fluid movement from the aqueous and vitreous humors into the bloodstream.

Pharmacodynamics

Glycerin is classified as an osmotic laxative, which acts to retain water in the fecal matter, softening stools and making them easier to pass. Its local irritant effects also contribute to its laxative properties. Glycerin suppositories typically produce a bowel movement within 15 to 30 minutes of administration.

Pharmacokinetics

Glycerin is readily absorbed from the gastrointestinal tract when taken orally and is metabolized primarily in the liver. It is distributed widely throughout the body, with excretion occurring primarily via the kidneys. The onset of action for glycerin when used as a laxative is relatively quick, particularly when used rectally.

Contra-indications

• Severe dehydration
• Severe renal impairment
• Intestinal obstruction
• Appendicitis

Adverse effects

• Abdominal cramps
• Diarrhea
• Nausea
• Vomiting
• Electrolyte imbalance

Interactions

• May enhance the effects of other laxatives
• Caution with concurrent use of diuretics due to potential electrolyte imbalance

Precautions

• Use with caution in patients with renal impairment
• Monitor electrolytes in patients with prolonged use
• Not recommended for long-term use

Pregnancy

Glycerin is generally considered safe during pregnancy but should be used under medical advice.

Breast-feeding

Glycerin is excreted in breast milk in small amounts and is considered safe for use while breastfeeding.

Storage

Store at room temperature, away from moisture and heat.

Formulations

• Glycerin suppositories
• Glycerin oral solution

Indications

• Oxidative stress-related conditions
• Inflammatory conditions
• Potential anti-aging applications
• Vascular health enhancement

Dosage

Children: Refer to specific product formulations and guidelines, as dosing can vary based on the concentration of hydrogen in the product used.

Adults: Refer to specific product formulations and guidelines, as dosing can vary based on the concentration of hydrogen in the product used.

Mechanism of action

Molecular hydrogen acts primarily as an antioxidant and anti-inflammatory agent. It is believed to exert its beneficial effects through the activation of the Nrf2 pathway, which enhances the expression of antioxidant enzymes and protects cells from oxidative stress. Hydrogen-rich environments have been shown to mitigate the harmful effects of various toxins on human umbilical vein endothelial cells, thereby promoting vascular health and longevity.

Pharmacodynamics

Hydrogen's pharmacodynamic properties are linked to its role as a potent antioxidant, which reduces reactive oxygen species (ROS) and modulates inflammation. It has been documented to counteract cellular senescence in endothelial cells, thereby maintaining vascular integrity and promoting overall health. The long-lasting effects of hydrogen exposure can be observed even after its concentration in the medium has decreased, suggesting a sustained activation of protective cellular pathways.

Pharmacokinetics

Hydrogen is a gaseous molecule that diffuses rapidly across biological membranes. Its absorption and distribution in the body are influenced by the method of administration, with hydrogen-rich water being a common delivery form. Once in the bloodstream, hydrogen is quickly utilized by tissues, and its concentration diminishes rapidly, with a half-life that can vary based on conditions. The elimination of hydrogen primarily occurs via exhalation, making it a non-toxic molecule with a favorable safety profile.

Pregnancy

Hydrogen is generally considered safe during pregnancy, but it is advisable to consult a healthcare provider for specific recommendations.

Breast-feeding

Hydrogen is considered safe during breastfeeding, but as with any substance, it is recommended to discuss with a healthcare provider.

Storage

Hydrogen should be stored in a cool, dry place away from direct sunlight and heat sources, in appropriate gas cylinders designed for compressed gases.

Formulations

• Hydrogen gas (H2)
• Hydrogen-rich water

Mechanism of action

Hydrogenphosphate acts as a substrate for various enzymatic reactions where phosphate groups are transferred or incorporated into organic molecules. It is involved in metabolic pathways such as nicotine biosynthesis and NAD/NADH cycling, facilitating biochemical reactions that are vital for cellular function.

Pharmacodynamics

Hydrogenphosphate is crucial for maintaining cellular homeostasis. It regulates acid-base balance and is involved in energy metabolism. The phosphate groups it provides are integral to the structure and function of ATP, which is the primary energy currency of the cell. Additionally, hydrogenphosphate influences signal transduction pathways through phosphorylation and dephosphorylation processes.

Pharmacokinetics

Hydrogenphosphate is readily absorbed in the gastrointestinal tract and distributed throughout the body. Its elimination primarily occurs through renal excretion, where it is filtered and reabsorbed by the kidneys. The balance of hydrogenphosphate levels is tightly regulated by various physiological mechanisms to ensure proper metabolic function.

Pregnancy

There is limited information regarding the safety of hydrogenphosphate in pregnancy. Consult relevant guidelines and consider potential risks versus benefits.

Breast-feeding

Data on the excretion of hydrogenphosphate in human milk are not available. Caution is advised.

Storage

Store in a cool, dry place away from direct sunlight. Ensure containers are tightly closed.

Indications

• Type 1 diabetes mellitus
• Type 2 diabetes mellitus
• Diabetic ketoacidosis (as part of a comprehensive treatment plan)

Dosage

Children: Refer to the BNF for Children for appropriate dosing guidelines for paediatric patients, considering factors such as age, weight, and specific medical conditions.

Adults: Refer to the BNF for specific dosing recommendations based on individual patient needs and blood glucose monitoring.

Mechanism of action

Isophane insulin works by promoting the uptake of glucose into cells, particularly in muscle and adipose tissue, while inhibiting hepatic glucose production. This action lowers blood glucose levels and helps to maintain glycemic control in diabetic patients. The onset of action typically occurs within 1 to 3 hours, with a peak effect at 4 to 12 hours, and a duration of action lasting up to 24 hours.

Pharmacodynamics

The pharmacodynamics of isophane involve the regulation of carbohydrate metabolism through insulin's ability to facilitate glucose transport across cell membranes. It also inhibits lipolysis and ketogenesis, promoting fat storage instead of fat breakdown. The overall effect is a decrease in blood glucose concentration, which is crucial for patients with diabetes who struggle with hyperglycemia.

Pharmacokinetics

Isophane insulin is administered subcutaneously, where it is absorbed into the bloodstream. The pharmacokinetics of isophane are characterized by a gradual absorption phase due to its formulation, which includes protamine to prolong the insulin's action. The time to peak plasma concentration typically occurs within 4 to 12 hours post-injection, and the elimination half-life varies based on individual metabolic factors and injection site.

Contra-indications

• Hypersensitivity to isophane or any of its components
• Severe hypoglycemia
• Diabetic ketoacidosis
• Conditions where a rapid correction of hyperglycemia is not advisable

Adverse effects

• Hypoglycemia
• Weight gain
• Injection site reactions (such as redness, swelling, or itching)
• Allergic reactions (such as rash, itching, or difficulty breathing)
• Lipodystrophy (localized loss of fat tissue at injection sites)
• Diabetic retinopathy progression

Interactions

• Other antidiabetic agents (e.g., sulfonylureas may increase the risk of hypoglycemia)
• Beta-blockers (can mask symptoms of hypoglycemia)
• Thiazide diuretics (may increase blood glucose levels)
• Corticosteroids (can increase blood glucose levels)
• Alcohol (can either potentiate or inhibit the hypoglycemic effect)

Precautions

• Ensure proper administration technique to avoid injection site complications
• Monitor blood glucose levels regularly
• Educate patients on signs and symptoms of hypoglycemia
• Adjust dosage based on lifestyle changes, such as diet and exercise

Pregnancy

Isophane can be used during pregnancy if the potential benefit justifies the potential risk to the fetus. Close monitoring of blood glucose levels is essential.

Breast-feeding

Isophane is excreted in breast milk, but the effects on the nursing infant are not well studied. Use caution and monitor the infant if the mother is using this medication.

Storage

Store in a refrigerator (2-8°C). Do not freeze. Once opened, isophane can be kept at room temperature for a limited time as specified by the manufacturer.

Formulations

• Isophane insulin suspension (NPH insulin) for subcutaneous use

Mechanism of action

Oxides do not have a single mechanism of action as they are a broad category of compounds. However, in general, metal oxides can exhibit catalytic properties, while non-metal oxides may participate in biochemical reactions by forming acids or bases upon dissolution in water.

Pharmacodynamics

The pharmacodynamics of oxides depend on the specific type of oxide and its interaction with biological systems. For instance, metal oxides may have antimicrobial properties, while certain non-metal oxides can influence metabolic pathways through their acid-base chemistry. The effects vary widely, necessitating specific studies for each oxide's role in therapeutic contexts.

Pharmacokinetics

The pharmacokinetics of oxides are also variable. Many metal oxides are poorly soluble and thus have limited absorption when ingested. Non-metal oxides, such as carbon dioxide, can be readily absorbed and utilized in metabolic processes. The distribution, metabolism, and excretion of oxides depend on their chemical form and the biological system in which they are involved.

Pregnancy

Not applicable as oxide is not a drug but a class of chemical compounds.

Breast-feeding

Not applicable as oxide is not a drug but a class of chemical compounds.

Storage

Store in a cool, dry place away from direct sunlight.

Mechanism of action

INSULIN HAS DIRECT INHIBITORY EFFECT ON LIPASE CONCERNED WITH MOBILIZATION OF FATTY ACIDS, WHILE GROWTH HORMONE, GLUCOCORTICOIDS, THYROID HORMONES & CATECHOLAMINES ENHANCE LIPOLYSIS. IN ABSENCE OF INSULIN THERE IS ABNORMALLY HIGH RATE OF CONVERSION OF PROTEIN TO GLUCOSE. ... PROTEINS & AMINO ACIDS ARE CONVERTED TO GLUCOSE @ ABNORMALLY HIGH RATE IN INSULIN DEFICIENCY. THE LIVER IS SITE OF CONVERSION. PROTEIN & AMINO ACIDS ARE MOBILIZED FROM PERIPHERAL TISSUES. INSULIN ACTS TO.../STIMULATE/ GLYCOGEN SYNTHESIS. MECHANISM OF IMPORTANT ACTIONS OF INSULIN TO ENHANCE FACILITATED DIFFUSION OF GLUCOSE & ACTIVE TRANSPORT OF AMINO ACIDS ARE NOT KNOWN.

Mechanism of action

Phenol is a potent proteolytic agent. Concentrations in the 5% to 7% range dissolve tissue on contact via proteolysis. In high concentrations when injected next to a nerve, phenol produces a chemical neurolysis which is nonselective across nerve fiber size and most prominent on its outer aspect. Local anesthetic effects occur within 5-10 minutes. The effects of monoamine depletors and monoamine denervators on phenol induced tremor were studied in mice. The tremor induced by phenol was enhanced by pretreatment with reserpine or tetrabenazine, but not with syrosingopine. However, alpha-methyl-p-tyrosine, p-chlorophenylalanine or 6-hydroxydopamine did not affect the tremor. These results suggest that the depletion of central monoamines as a whole contribute to the enhancement of the tremor induced by phenol.

Mechanism of action

When administered rectally, glycerin exerts a hygroscopic and/or local irritant action, drawing water from the tissues into the feces and reflexively stimulating evacuation. Glycerin decreases intraocular pressure by creating an osmotic gradient between the blood and intraocular fluid, causing fluid to move out of the aqueous and vitreous humors into the bloodstream. Glycerin (glycerol) and sorbitol are hyperosmotic laxatives. When administered rectally, glycerin and sorbitol exert a hygroscopic and/or local irritant action, drawing water from the tissues into the feces and reflexly stimulating evacuation. The extent to which the simple physical distention of the rectum and the hygroscopic and/or local irritant actions are responsible for the laxative effects of some of these drugs is not known. Only extremely high oral doses of sorbitol (25 g daily) or glycerin exert laxative action. /Glycerin/ decreases intraocular pressure by creating an osmotic gradient between the blood and intraocular fluid, causing fluid to move out of the aqueous and vitreous humors into the bloodstream. The physicochemical effects of a series of alkanols, alkanediols and glycerol on erythrocyte shape and hemolysis at 4 and 20 degrees C were examined. We calculated the dielectric constant of the incubation medium, Ds, and the dielectric constant of the erythrocyte membrane Dm in the presence of organic solutes. The ratio Ds/Dm = -38.48 at 20 degrees C defines the normal biconcave shape in a medium without hemolytic agents. A decrease in Ds/Dm favors externalization or internalization with consequent hemolysis. Alkanols and alkanediols convert biconcave erythrocytes into echinocytes, which is accompanied by an increase in the projected surface area. Glycerol converts biconcave erythrocytes into stomatocytes, which was accompanied by a marginal decrease in the projected surface area. Progressive externalization in alkanols and alkanediols or internalization in glycerol resulted in a decrease in the projected surface area and the formation of smooth spheres. The degree of shape change induced was related to the degree of hemolysis and the ratio Ds/Dm. A decrease in temperature reduced both the degree of shape change and hemolysis. .../Thus/ physicochemical toxicity may be a result of a temperature dependent hydrophobic interaction between the organic solutes and the membrane and is best interpreted by the ability of the solutes to change Ds and Dm.

Pharmacodynamics

Glycerin is commonly classified as an osmotic laxative but may act additionally or alternatively through its local irritant effects; it may also have lubricating and fecal softening actions. Glycerin suppositories usually work within 15 to 30 minutes.

Mechanism of action

Substantial evidence indicates that molecular hydrogen (H2) has beneficial vascular effects because of its antioxidant and/or anti-inflammatory effects. Thus, hydrogen-rich water may prove to be an effective anti-aging drink. This study examined the effects of H2 on endothelial senescence and clarified the mechanisms involved. Hydrogen-rich medium was produced by a high-purity hydrogen gas generator. Human umbilical vein endothelial cells (HUVECs) were incubated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for various time periods in normal or hydrogen-rich medium. The baseline H2concentration in hydrogen-rich medium was 0.55 +/- 0.07 mmol/L. This concentration gradually decreased, and H2 was almost undetectable in medium after 12 hr. At 24 hr after TCDD exposure, HUVECs treated with TCDD exhibited increased 8OHdG and acetyl-p53 expression, decreased nicotinamide adenine dinucleotide (NAD(+))/NADH ratio, impaired Sirt1 activity, and enhanced senescence-associated beta-galactosidase. However, HUVECs incubated in hydrogen-rich medium did not exhibit these TCDD-induced changes accompanying Nrf2 activation, which was observed even after H2 was undetectable in the medium. Chrysin, an inhibitor of Nrf2, abolished the protective effects of H2 on HUVECs. H2 has long-lasting antioxidant and anti-aging effects on vascular endothelial cells through the Nrf2 pathway, even after transient exposure to H2. Hydrogen-rich water may thus be a functional drink that increases longevity. /Hydrogen-rich water/ Amyloid beta (Abeta) peptides are identified /as a/ cause of neurodegenerative diseases such as Alzheimer's disease (AD). Previous evidence suggests Abeta-induced neurotoxicity is linked to the stimulation of reactive oxygen species (ROS) production. The accumulation of Abeta-induced ROS leads to increased mitochondrial dysfunction and triggers apoptotic cell death. This suggests antioxidant therapies may be beneficial for preventing ROS-related diseases such as AD. Recently, hydrogen-rich water (HRW) has been proven effective in treating oxidative stress-induced disorders because of its ROS-scavenging abilities. However, the precise molecular mechanisms whereby HRW prevents neuronal death are still unclear. In the present study, we evaluated the putative pathways by which HRW protects against Abeta-induced cytotoxicity /in SK-N-MC cells/. Our results indicated that HRW directly counteracts oxidative damage by neutralizing excessive ROS, leading to the alleviation of Abeta-induced cell death. In addition, HRW also stimulated AMP-activated protein kinase (AMPK) in a sirtuin 1 (Sirt1)-dependent pathway, which upregulates forkhead box protein O3a (FoxO3a) downstream antioxidant response and diminishes Abeta-induced mitochondrial potential loss and oxidative stress. Taken together, our findings suggest that HRW may have potential therapeutic value to inhibit Abeta-induced neurotoxicity. /Hydrogen-rich water/ The NLRP3 inflammasome, an intracellular multi-protein complex controlling the maturation of cytokine interleukin-1beta, plays an important role in lipopolysaccharide (LPS)-induced inflammatory cascades. Recently, the production of mitochondrial reactive oxygen species (mtROS) in macrophages stimulated with LPS has been suggested to act as a trigger during the process of NLRP3 inflammasome activation that can be blocked by some mitochondria-targeted antioxidants. Known as a ROS scavenger, molecular hydrogen (H2) has been shown to possess therapeutic benefit on LPS-induced inflammatory damage in many animal experiments. Due to the unique molecular structure, H2 can easily target the mitochondria, suggesting that H2 is a potential antagonist of mtROS-dependent NLRP3 inflammasome activation. Here we have showed that, in mouse macrophages, H2 exhibited substantial inhibitory activity against LPS-initiated NLRP3 inflammasome activation by scavenging mtROS. Moreover, the elimination of mtROS by H2 resultantly inhibited mtROS-mediated NLRP3 deubi