Skeletal muscle is primarily involved in exercise performance and health promotion. Sulforaphane (SFN) is a naturally occurring isothiocyanate that indirectly activates the transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2), thus inducing the expression of Nrf2 target genes, including antioxidant enzymes. This study aimed to identify the effects of a single dose of SFN administration on exhaustive exercise-induced inflammation and oxidative stress in skeletal muscle tissue and elucidate the underlying mechanisms. Thirty-six mice were divided into four groups: control, SFN, exercise (Ex), and SFN + Ex. The SFN group and SFN + Ex group received SFN orally (50 mg/kg body weight) 2 h before the running test. Exercise significantly reduced plasma glucose levels, while the SFN-treated group exhibited a smaller reduction. Acute exhaustive exercise increased the expression of pro-inflammatory cytokines in muscle tissue, while the SFN + Ex group exhibited significantly reduced expression of pro-inflammatory cytokines. The gene expression of Nrf2 and its target enzymes, including heme oxygenase (HO)-1, superoxide dismutase (SOD)-1, catalase (CAT), and glutathione peroxidase (GPx)-1, was measured in the gastrocnemius and soleus muscle tissue. Compared with the Ex group, the SFN + Ex group showed upregulated expression of all these parameters, including Nrf2. SFN treatment reduced acute exhaustive exercise-induced oxidative stress and inflammation via activation of the Nrf2/HO-1 signaling pathway.

With the development of medicine and chemistry, an increasing number of plant-derived medicines have been shown to exert beneficial therapeutic on the treatment of various physical and psychological diseases. In particular, by using physical chemistry methods, we are able to examine the chemical components of plants and the effects of these substances on the human body. Muscle atrophy (MA) is characterized by decreased muscle mass and function, is caused by multiple factors and severely affects the quality of life of patients. The multifactorial and complex pathogenesis of MA hinders drug research and disease treatment. However, phytotherapy has achieved significant results in the treatment of MA. We searched PubMed and the Web of Science for articles related to plant-derived substances and muscle atrophy. After applying exclusion and inclusion criteria, 166 and 79 articles met the inclusion criteria, respectively. A total of 173 articles were included in the study after excluding duplicates. The important role of phytoactives such as curcumin, resveratrol, and ginsenosides in the treatment of MA (e.g., maintaining a positive nitrogen balance in muscles and exerting anti-inflammatory and antioxidant effects) has been extensively studied. Unfortunately, MA dose not have to a single cause, and each cause has its own unique mechanism of injury. This review focuses on the therapeutic mechanisms of active plant components in MA and provides insights into the personalized treatment of MA.

Skeletal muscle tissue can regenerate after damage through the action of satellite cells, which proliferate as myoblasts when activated. Oxidative stress, marked by high rates of reactive oxygen species (e.g., hydrogen peroxide, H2O2), impairs this process by increasing myoblast cell death. Moringa oleifera leaf extract (MOLE), known for its antioxidant properties, was tested for its protective effects on C2C12 myoblasts under oxidative stress. We assessed MOLE's impact on total antioxidant capacity (TAC), glutathione homeostasis (GSH/GSSG), cell viability, and wound recovery. The metabolomic analysis of MOLE using an LC-MSMS ZenoTOF 7600 mass spectrometry system identified key compounds, including peculiar glucosinolates (42.1%) and flavonoids (18.8%), as well as phenolic acids (4.5%) and other significant metabolites (34.6%; among them, amino acids, vitamins, and fatty acids). H2O2 disrupted myoblast redox balance and caused cell death, but MOLE treatment restored the GSH/GSSG ratio, improved TAC, and increased cell viability. Additionally, MOLE promoted faster wound closure in myoblasts exposed to H2O2. These findings suggest that MOLE can protect C2C12 myoblasts by restoring redox balance and enhancing recovery under oxidative stress.

Sulforaphane (SFN) has been demonstrated to exert a protective role in various diseases. However, the role of SFN in phosgene-induced acute lung injury (P-ALI) remains unclear. This study aimed to explore the role and mechanism of SFN in P-ALI and provide a theoretical basis for the clinical prevention and treatment of P-ALI.

A mouse model of P-ALI was established followed by phosgene gas inhalation at a dose of 4.17 g/m3 for 5 min. The survival rate, lung coefficient and hematoxylin and eosin (H&E) staining, lung pathology scoring, and bronchoalveolar lavage fluid (BALF) analysis were performed to evaluate lung tissue damage. The real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting analysis were utilized to evaluate the relative expression levels of inflammation factors and protein expression.

Compared with the control group, destruction of alveolar structure, pulmonary edema, lung tissue inflammation and oxidative stress occurred after phosgene exposure. After the administration of SFN, the massive exudation of red blood cells and significant thickening of alveolar interstitium were ameliorated, the lung tissue inflammation was improved, and oxidative stress level was reduced. Mechanically, SFN could increase the expression of nuclear factor erythroid 2 (NFE2)-related factor 2 (Nrf2) protein and the downstream heme oxgenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1), thereby improving P-ALI. And the Nrf2 inhibitor ML385 attenuated the lung protective effect of SFN.

Phosgene inhalation led to edema, inflammation, and oxidative stress of lung tissue in mice. SFN might ameliorate phosgene-induced lung injury through Nrf2-HO-1/NQO1 signaling pathway.

Neuropathic pain, a chronic condition resulting from nerve injury or dysfunction, presents significant therapeutic challenges and is closely associated with oxidative stress and inflammation, both of which can lead to mitochondrial dysfunction. The nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, a critical cellular defense mechanism against oxidative stress, has emerged as a promising target for neuropathic pain management. Nrf2 modulators enhance the expression of antioxidant and cytoprotective genes, thereby reducing oxidative damage, inflammation, and mitochondrial impairment. This review explores the antinociceptive effects of Nrf2, highlighting how pharmacological agents and natural compounds may be used as potential therapeutic strategies against neuropathic pain. Although preclinical studies demonstrate significant pain reduction and improved nerve function through Nrf2 activation, several clinical challenges need to be addressed. However, emerging clinical evidence suggests potential benefits of Nrf2 modulators in several conditions, such as diabetic neuropathy and multiple sclerosis. Future research should focus on further elucidating the molecular role of Nrf2 in neuropathic pain to optimize its modulation efficacy and maximize clinical utility.

Moringa oleifera is widely grown throughout the tropics and increasingly used for its therapeutic and nutraceutical properties. These properties are attributed to potent antioxidant and metabolism regulators, including glucosinolates/isothiocyanates as well as flavonoids, polyphenols, and phenolic acids. Research to date largely consists of geographically limited studies that only examine material available locally. These practices make it unclear as to whether moringa samples from one area are superior to another, which would require identifying superior variants and distributing them globally. Alternatively, the finding that globally cultivated moringa material is essentially functionally equivalent means that users can easily sample material available locally. We brought together accessions of Moringa oleifera from four continents and nine countries and grew them together in a common garden. We performed a metabolomic analysis of leaf extracts (MOLE) using an LC-MSMS ZenoTOF 7600 mass spectrometry system. The antioxidant capacity of leaf samples evaluated using the Total Antioxidant Capacity assay did not show any significant difference between extracts. MOLE samples were then tested for their antioxidant activity on C2C12 myotubes challenged with an oxidative insult. Hydrogen peroxide (H2O2) was added to the myotubes after pretreatment with different extracts. H2O2 exposure caused an increase in cell death that was diminished in all samples pretreated with moringa extracts. Our results show that Moringa oleifera leaf extract is effective in reducing the damaging effect of H2O2 in C2C12 myotubes irrespective of geographical origin. These results are encouraging because they suggest that the use of moringa for its therapeutic benefits can proceed without the need for the lengthy and complex global exchange of materials between regions.

Sulforaphane (SFN) is a promising molecule for developing phytopharmaceuticals due to its potential antioxidative and anti-inflammatory effects. A plethora of research conducted in vivo and in vitro reported the beneficial effects of SFN intervention and the underlying cellular mechanisms. Since SFN is a newly identified nutraceutical in sports nutrition, only some human studies have been conducted to reflect the effects of SFN intervention in exercise-induced inflammation and oxidative stress. In this review, we briefly discussed the effects of SFN on exercise-induced inflammation and oxidative stress. We discussed human and animal studies that are related to exercise intervention and mentioned the underlying cellular signaling mechanisms. Since SFN could be used as a potential therapeutic agent, we mentioned briefly its synergistic attributes with other potential nutraceuticals that are associated with acute and chronic inflammatory conditions. Given its health-promoting effects, SFN could be a prospective nutraceutical at the forefront of sports nutrition.

Oxidative stress plays a vital role for the adaptive responses to physical training. However, excessive oxidative stress can precipitate cellular damage, necessitating protective mechanisms to mitigate this effect. Glucosinolates, found predominantly in cruciferous vegetables, can be converted into isothiocyanates, known for their antioxidative properties. These compounds activate crucial antioxidant defence pathways and support mitochondrial function and protein integrity under oxidative stress, in both Nrf2-dependent and independent manners. We here administered glucosinolate-rich broccoli sprouts (GRS), in a randomized double-blinded cross-over fashion to 9 healthy subjects in combination with daily intense exercise training for 7 days. We found that exercise in combination with GRS significantly decreased the levels of carbonylated proteins in skeletal muscle and the release of myeloperoxidase into blood. Moreover, it lowered lactate accumulation during submaximal exercise, and attenuated the severe nocturnal hypoglycaemic episodes seen during the placebo condition. Furthermore, GRS in combination with exercise improved physical performance, which was unchanged in the placebo condition.

There is a clear relationship between quantitative measures of fitness (e.g., VO₂ max) and outcomes after surgical procedures. Whether or not fitness is a modifiable risk factor and what underlying biological processes drive these changes are not known. The purpose of this study was to evaluate the moderate exercise training effect on sepsis outcomes (survival) as well as the hepatic biological response. We chose to study the liver because it plays a central role in the regulation of immune defense during systemic infection and receives blood flow directly from the origin of infection (gut) in the cecal ligation and puncture (CLP) model.

We randomized 50 male (♂) and female (♀) Sprague-Dawley rats (10 weeks, 340 g) to 3 weeks of treadmill exercise training, performed CLP to induce polymicrobial "sepsis," and monitored survival for five days (Part I). In parallel (Part II), we randomized 60 rats to control/sedentary (G1), exercise (G2), exercise + sham surgery (G3), CLP/sepsis (G4), exercise + CLP [12 h (G5) and 24 h (G6)], euthanized at 12 or 24 h, and explored molecular pathways related to exercise and sepsis survival in hepatic tissue and serum.

Three weeks of exercise training significantly increased rat survival following CLP (polymicrobial sepsis). CLP increased inflammatory markers (e.g., TNF-a, IL-6), which were attenuated by exercise. Sepsis suppressed the SOD and Nrf2 expression, and exercise before sepsis restored SOD and Nrf2 levels near the baseline. CLP led to increased HIF1a expression and oxidative and nitrosative stress, the latter of which were attenuated by exercise. Haptoglobin expression levels were increased in CLP animals, which was significantly amplified in exercise + CLP (24 h) rats.

Moderate exercise training (3 weeks) increased the survival in rats exposed to CLP, which was associated with less inflammation, less oxidative and nitrosative stress, and activation of antioxidant defense pathways.

Muscle fatigue is defined as a decrease in maximal force or power generated in response to contractile activity, and it is a risk factor for the development of musculoskeletal injuries. One of the many stressors imposed on skeletal muscle through exercise is the increased production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), which intensifies as a function of exercise intensity and duration. Exposure to ROS/RNS can affect Na⁺/K⁺-ATPase activity, intramyofibrillar calcium turnover and sensitivity, and actin-myosin kinetics to reduce muscle force production. On the other hand, low ROS/RNS concentrations can likely upregulate an array of cellular adaptative responses related to mitochondrial biogenesis, glucose transport and muscle hypertrophy. Consequently, growing evidence suggests that exogenous antioxidant supplementation might hamper exercise-engendering upregulation in the signaling pathways of mitogen-activated protein kinases (MAPKs), peroxisome-proliferator activated co-activator 1α (PGC-1α), or mammalian target of rapamycin (mTOR). Ultimately, both high (exercise-induced) and low (antioxidant intervention) ROS concentrations can trigger beneficial responses as long as they do not override the threshold range for redox balance. The mechanisms underlying the two faces of ROS/RNS in exercise, as well as the role of antioxidants in muscle fatigue, are presented in detail in this review.

Sulforaphane (SFN), an isothiocyanate derived from glucoraphanin, has antioxidant, and anti-inflammatory effects that may be beneficial for improving liver function. However, few studies regarding the effects of glucoraphanin on the biological markers related to liver function, such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyltransferase (γ-GTP) in healthy individuals have been reported. This randomized, double-blind, placebo-controlled parallel- group trial was conducted from April 22 to December 25, 2021 and compared the effects of broccoli sprout supplements enriched in glucoraphanin (glucoraphanin supplements) (n = 35) with those of placebo supplements (n = 35). This trial was registered with the University Hospital Medical Information Network Clinical Trial Registry (UMIN-CTR; ID number UMIN000044005) https://center6.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view. cgi?recptno=R000050252. Glucoraphanin significantly improved serum ALT levels at 24 weeks compared to placebo supplements. However, no significant difference in serum glutathione levels, one of the major antioxidants synthesized in the liver, was observed between the two groups. In conclusion, daily intake of the glucoraphanin supplements is beneficial for maintaining liver health in healthy, middle-aged adults with high-normal serum hepatic biomarkers, although further studies focusing on other antioxidant markers are needed to understand how glucoraphanin improves liver function.

The practice of physical exercise induces a series of physiological changes in the body at different levels, either acutely or chronically. During exercise, the increase in oxygen consumption promotes the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), which are necessary to maintain homeostasis. ROS/RNS activate cellular signaling pathways, such as the antioxidant cytoprotective systems, inflammation, and cell proliferation, which are crucial for cell survival. However, in exhaustive-extended physical exercise, workloads can exceed the endogenous antioxidant defenses, which may be related to impairment of muscle contraction, fatigue, and a decrease in athletic performance. This review addresses the role of some antioxidants from plant-derived extracts called phytochemicals that can mediate the response to oxidative stress induced by physical exercise by activating signaling pathways, such as Nrf2/Keap1/ARE, responsible for the endogenous antioxidant response and possibly having an impact on sports performance.

The mobility of the human body depends on, among other things, muscle health, which can be affected by several situations, such as aging, increased oxidative stress, malnutrition, cancer, and the lack or excess of physical exercise, among others. Genetic, metabolic, hormonal, and nutritional factors are intricately involved in maintaining the balance that allows proper muscle function and fiber recovery; therefore, the breakdown of the balance among these elements can trigger muscle atrophy. The study from the nutrigenomic perspective of nutritional factors has drawn wide attention recently; one of these is the use of certain compounds derived from foods and plants known as phytochemicals, to which various biological activities have been described and attributed in terms of benefiting health in many respects. This work addresses the effect that the phytochemicals curcumin from Curcuma longa Linn and sulforaphane from Brassicaceae species have shown to exert on muscle function, recovery, and the prevention of muscle atrophy, and describes the impact on muscle health in general. In the same manner, there are future perspectives in research on novel compounds as potential agents in the prevention or treatment of medical conditions that affect muscle health.