As a derivative of flavonoids, the expansion of the anti-inflammatory and antioxidant activities of hidrosmin is an important direction in the field of pharmacology, which not only deepens the understanding of its molecular mechanism, but also provides the basis for its potential applications in a variety of diseases. The following is a description of the specific research content, mechanism analysis and application scenarios:
I. Expansion of anti-inflammatory activity
The anti-inflammatory effect of hidrosmin is not limited to a single target or disease model, but rather, it shows its potential in different inflammation-related scenarios through the modulation of multiple pathways and dimensions:
Precise regulation of inflammatory signaling pathways:
study found that it can specifically inhibit the activation of the NF-κB (nuclear factor -κB) pathway — the pathway is the “core switch” of the inflammatory response, and over-activation leads to the activation of pro-inflammatory cytokines such as TNF-α, IL-6. IL- 1β, and so on. 1β and other pro-inflammatory cytokines to be released in large quantities. Hidrosmin reduces the transcription of downstream inflammatory factors by blocking the transfer of NF-κB from the cytoplasm to the nucleus, thereby reducing the extent of acute inflammation (e.g., postoperative swelling) and chronic inflammation (e.g., rheumatoid arthritis).
Meanwhile, its inhibitory effect on MAPK (mitogen-activated protein kinase) family (e.g. p38. JNK) can further block the cascade amplification of inflammatory signals and enhance the anti-inflammatory effect.
Regulation of specific inflammatory cells:
In chronic inflammation, the polarization state of macrophages (M1-type pro-inflammatory / M2-type anti-inflammatory) is key. Hidrosmin promotes the conversion of macrophages to the M2 type, reducing the secretion of inflammatory mediators (e.g., nitric oxide, prostaglandin E2) and increasing the release of anti-inflammatory factors (e.g., IL-10), thus realizing the effect of “suppression of inflammation at the source”. This mechanism allows it to show intervention potential in disease models such as inflammatory bowel disease (e.g. ulcerative colitis) and skin inflammation (e.g. eczema).
Explore applications in clinically relevant inflammation scenarios:
Post-operative inflammation: investigate its role in alleviating soft tissue swelling and pain after orthopedic surgery, accelerating recovery by inhibiting localized inflammatory exudation.
Respiratory inflammation: in asthma or chronic obstructive pulmonary disease (COPD) models, it reduces airway smooth muscle contraction and mucus secretion, alleviating airway inflammation and spasm.
Second, the multi-dimensional extension of antioxidant activity
The antioxidant ability of hidrosmin is not only reflected in the direct scavenging of free radicals, but also through the regulation of the body’s antioxidant system, to deal with a variety of oxidative stress-related damage:
Free radical scavenging and lipid peroxidation inhibition:
As a flavonoid, the phenolic hydroxyl group in its molecular structure can directly bind with hydroxyl radical (・OH), superoxide anion (O₂-・) and other reactive oxygen species (ROS), and terminate the free radical chain reaction. At the same time, it can inhibit the generation of lipid peroxidation products (e.g. malondialdehyde) and protect the structural integrity of cell membranes, a property that has enabled it to show its protective effects in models of myocardial ischemia/reperfusion injury, liver injury, etc. – for example, when blood flow is restored after myocardial ischemia, the oxidative damage to cardiomyocytes caused by ROS can be reduced, and the infarcted area of the heart can be lowered. .
Activation of the body’s antioxidant system:
It can upregulate the activity of endogenous antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and enhance the body’s own antioxidant capacity. In models of neurodegenerative diseases (e.g., Alzheimer’s disease), this effect reduces neuronal damage by ROS, protects synaptic function, and delays cognitive decline.
Association studies with oxidative stress-related diseases:
Diabetic complications: Hyperglycemia induces oxidative stress, leading to tissue damage in blood vessels, kidneys, and other tissues. Hidrosmin may improve glomerular filtration function and reduce proteinuria in diabetic nephropathy patients through antioxidant effects.
Skin photoaging: ROS generated by UV radiation is an important causative factor of skin aging, which can slow down the formation of skin wrinkles and loss of elasticity by scavenging ROS and inhibiting the degradation of collagen by matrix metalloproteinases (MMPs).