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Epilepsy, a chronic neurological disorder affecting millions globally, is often exacerbated by neuroinflammation and oxidative stress. Existing antiepileptic drugs primarily manage symptoms, leaving the disease's progression largely unaddressed. Flavonoids, ubiquitous plant metabolites with potent antiinflammatory and antioxidant properties, show promise in epilepsy treatment. Unlike conventional therapies, they targetmultiple pathophysiological processes simultaneously, offering a comprehensive approach to this complex neurological disorder. This review explores the dual role of flavonoids in mitigating neuroinflammation and reducing oxidative stress through various molecular pathways. By inhibiting key inflammatory mediators and pathways such as NF-κB, MAPK, JNK, and JAK, flavonoids offer neuronal protection. They enhance the body's natural antioxidant defenses by modulating enzyme activities, including superoxide dismutase, catalase, and glutathione peroxidase. Moreover, flavonoids influence crucial antioxidant response pathways like PI3K/AKT, Nrf2, JNK, and PKA. Despite their therapeutic promise, the low bioavailability of flavonoids poses a considerable challenge. However, cutting-edge strategies, including nanotechnology and chemical modifications, are underway to improve their bioavailability and therapeutic efficacy. These advancements support the potential of flavonoids as a valuable addition to epilepsy treatment strategies. [ABSTRACT FROM AUTHOR]

Coronary heart disease (CHD) is the most common clinical manifestation of cardiovascular disease. It is characterized by myocardial ischemia, which is caused by coronary atherosclerosis. CHD is a significant global health problem with increasing prevalence every year because of significant changes in the lifestyles and diets. Ginseng is a traditional Chinese medicinal herb that has been used in food preparations and traditional medicine for several centuries. Several studies have demonstrated that ginseng improved cardiac function by normalizing blood glucose levels and decreasing blood pressure, oxidative stress, platelet aggregation, and lipid dysregulation in vivo. This review describes the current understanding of the mechanisms by which ginseng alleviates CHD, and provides a reference for the clinical development and application of ginseng as an alternative therapy for CHD. [ABSTRACT FROM AUTHOR]

Astaxanthin (ASX) is a kind of carotenoid widely distributed in nature, which has been shown to extremely strong antioxidative effects and significant preventive and therapeutic effects on cancer, diabetes, cardiovascular disease, etc. However, its application in the medical field is greatly limited due to its poor water solubility, unstable chemical properties and other shortcomings. In recent years, the nanobased drug delivery systems such as nanoparticles, liposomes, nanoemulsions, nanodispersions, and polymer micelles, have been used as Astaxanthin delivery carriers with great potential for clinical applications, which have been proved that they can enhance the stability and efficacy of Astaxanthin and achieve targeted delivery of Astaxanthin. Herein, based on the pharmacological effects of Astaxanthin, we reviewed the characteristics of various drug delivery carriers, which is of great significance for improving the bioavailability of Astaxanthin. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the neuroprotective effect of resveratrol (RES) in rat models of cerebral ischemia/reperfusion (I/R) injury. Data sources: PubMed, Embase, MEDLINE, Cochrane Library, and Chinese databases were searched from their inception dates to July 2022. No language restriction was used in the literature search. Date Selection: Studies were selected that RES were used to treat cerebral I/R injury in vivo. Two reviewers conducted literature screening, data extraction and methodological quality assessment independently. Outcome measures: Cerebral infarct volume was included as primary outcome. The secondary outcomes included cerebral water content and neurological deficit scores. Malondialdehyde (MDA) and superoxide dismutase (SOD) were used to evaluate oxidative stress during medication. Results: A total of 41 studies were included, and only a few of them the methodological quality was relatively low. Compared with the control group, RES significantly reduced the cerebral infarct volume (29 studies, standard mean difference (SMD) = -2.88 [-3.23 to -2.53], p < 0.00001) and brain water content (nine studies, MD = -9.49 [-13.58 to -5.40], p < 0.00001) after cerebral I/R injury, then neurological function was improved (15 studies, SMD = -1.96 [-2.26 to -1.65], p < 0.00001). The MDA level (six studies, SMD = -8.97 [-13.60 to -4.34], p = 0.0001) was decreased notably after treatment of RES, while the SOD level (five studies, SMD = 3.13 [-0.16 to 6.43], p = 0.06) was increased unsatisfactory. Consistently, subgroup analysis of cerebral infarct volume suggested that the optimal therapeutic dose is 30 mg/kg (eight studies, SMD = -5.83 [-7.63 to -4.04], p < 0.00001). Meanwhile, 60 min of occlusion (three studies, SMD = -10.89 [-16.35 to -5.42], p < 0.0001) could get maximum benefit from compared with 90 min and 120 min of occlusion. On the other hand, the publication bias cannot be ignored. The pharmacological mechanisms of RES on cerebral I/R injury models as reported have be summarized, which can be used for reference by researchers to further plan their future experiments. Conclusion: RES might have a good neuroprotective effect on cerebral I/R injury in rats, then 30 mg/kg RES may be the optimal dose for treatment, and early administration of RES should be more neuroprotective. Also it need to be further verified through exploration of dose effect relationship, or delay administration or not. [ABSTRACT FROM AUTHOR]

Neuroinflammation is a protective mechanism against insults from exogenous pathogens and endogenous cellular debris and is essential for reestablishing homeostasis in the brain. However, excessive prolonged neuroinflammation inevitably leads to lesions and disease. The use of natural compounds targeting pathways involved in neuroinflammation remains a promising strategy for treating different neurological and neurodegenerative diseases. Astaxanthin, a natural xanthophyll carotenoid, is a well known antioxidant. Mounting evidence has revealed that astaxanthin is neuroprotective and has therapeutic potential by inhibiting neuroinflammation, however, its functional roles and underlying mechanisms in modulating neuroinflammation have not been systematically summarized. Hence, this review summarizes recent progress in this field and provides an update on the medical value of astaxanthin. Astaxanthin modulates neuroinflammation by alleviating oxidative stress, reducing the production of neuroinflammatory factors, inhibiting peripheral inflammation and maintaining the integrity of the blood-brain barrier. Mechanistically, astaxanthin scavenges radicals, triggers the Nrf2-induced activation of the antioxidant system, and suppresses the activation of the NF-κB and mitogen-activated protein kinase pathways. With its good biosafety and high bioavailability, astaxanthin has strong potential for modulating neuroinflammation, although some outstanding issues still require further investigation. [ABSTRACT FROM AUTHOR]

Benincasa hispida Cogn. (B. hispida) is a popular vegetable in China, and studies have been reported on B. hispida polysaccharides (BPS) preparation. However, few studies have been reported on its physicochemical and skincare properties. In this study, we analyzed the physicochemical properties of BPS, free radical scavenging capability, moisturizing and antioxidant activities in vitro and in vivo , respectively. Our results show that BPS was an inhomogeneous acidic polysaccharide that could scavenge a variety of free radicals. Also, BPS had a good moisturizing and antioxidant capability both in vitro and in vivo. Specifically, BPS could alter some key antioxidant enzyme activities and pro-inflammatory factor levels via activating the NRF2/HO-1 pathway, thereby preventing H2O2-induced reactive oxygen species (ROS) production and apoptosis of HDF-1 cells. Our results suggest that BPS exhibited favorable moisturizing and anti-aging properties and might be an attractive candidate for the development of anti-aging skincare products. [ABSTRACT FROM AUTHOR]

Background and Aims: Myocardial infarction (MI) is the clinical manifestation of atherosclerotic coronary artery disease. Spirulina is an algae known to ameliorate cardiometabolic disorders and with proven anti-inflammatory and anti-oxidant effects. We investigated, in a highly translatable animal model, whether oral supplementation with spirulina protects against the deleterious effects triggered by ST-elevation MI (STEMI). Methods: Pigs were fed a regular diet supplemented with spirulina (1 g/animal/bid) or placebo-control for 10 days. Thereafter, animals were subjected to 1.5 h percutaneous balloon-induced coronary occlusion (STEMI) followed by 2.5 h reperfusion and then sacrificed. We assessed infarct size and cardiac function. Blood samples and infarcted and remote myocardial tissue were obtained. Results: Spirulina supplementation reduced infarct size by 64%, increased myocardial salvage by 18%, and improved cardiac function by 30% vs. controls (p < 0.05). These benefits were associated with attenuation in DNA-oxidative damage and apoptotic markers and increased iNOS in the infarcted myocardium, higher AMPK activation in the remote myocardium, and lower myocardial MCP-1 expression. Systemically, spirulina attenuated Cox-2 expression in STEMI-activated peripheral blood mononuclear cells and enhanced TNF-α release acutely post-STEMI. Additionally, spirulina decreased weight gain progression over time (p < 0.05) without changes in lipids, glucose, liver or kidney parameters. Conclusion: A 10-day supplementation with spirulina exerts cardioprotection in a preclinical setting of STEMI by limiting cardiac damage and improving ventricular contractility through anti-oxidative, anti-inflammatory, and anti-apoptotic mechanisms. [ABSTRACT FROM AUTHOR]

Neuroinflammation is a protective mechanism against insults from exogenous pathogens and endogenous cellular debris and is essential for reestablishing homeostasis in the brain. However, excessive prolonged neuroinflammation inevitably leads to lesions and disease. The use of natural compounds targeting pathways involved in neuroinflammation remains a promising strategy for treating different neurological and neurodegenerative diseases. Astaxanthin, a natural xanthophyll carotenoid, is a well known antioxidant. Mounting evidence has revealed that astaxanthin is neuroprotective and has therapeutic potential by inhibiting neuroinflammation, however, its functional roles and underlying mechanisms in modulating neuroinflammation have not been systematically summarized. Hence, this review summarizes recent progress in this field and provides an update on the medical value of astaxanthin. Astaxanthin modulates neuroinflammation by alleviating oxidative stress, reducing the production of neuroinflammatory factors, inhibiting peripheral inflammation and maintaining the integrity of the blood-brain barrier. Mechanistically, astaxanthin scavenges radicals, triggers the Nrf2-induced activation of the antioxidant system, and suppresses the activation of the NF-κB and mitogen-activated protein kinase pathways. With its good biosafety and high bioavailability, astaxanthin has strong potential for modulating neuroinflammation, although some outstanding issues still require further investigation.

Benincasa hispida Cogn. (B. hispida) is a popular vegetable in China, and studies have been reported on B. hispida polysaccharides (BPS) preparation. However, few studies have been reported on its physicochemical and skincare properties. In this study, we analyzed the physicochemical properties of BPS, free radical scavenging capability, moisturizing and antioxidant activities in vitro and in vivo, respectively. Our results show that BPS was an inhomogeneous acidic polysaccharide that could scavenge a variety of free radicals. Also, BPS had a good moisturizing and antioxidant capability both in vitro and in vivo. Specifically, BPS could alter some key antioxidant enzyme activities and pro-inflammatory factor levels via activating the NRF2/HO-1 pathway, thereby preventing H2O2-induced reactive oxygen species (ROS) production and apoptosis of HDF-1 cells. Our results suggest that BPS exhibited favorable moisturizing and anti-aging properties and might be an attractive candidate for the development of anti-aging skincare products.

Background and Aims: Myocardial infarction (MI) is the clinical manifestation of atherosclerotic coronary artery disease. Spirulina is an algae known to ameliorate cardiometabolic disorders and with proven anti-inflammatory and anti-oxidant effects. We investigated, in a highly translatable animal model, whether oral supplementation with spirulina protects against the deleterious effects triggered by ST-elevation MI (STEMI).Methods: Pigs were fed a regular diet supplemented with spirulina (1 g/animal/bid) or placebo-control for 10 days. Thereafter, animals were subjected to 1.5 h percutaneous balloon-induced coronary occlusion (STEMI) followed by 2.5 h reperfusion and then sacrificed. We assessed infarct size and cardiac function. Blood samples and infarcted and remote myocardial tissue were obtained.Results: Spirulina supplementation reduced infarct size by 64%, increased myocardial salvage by 18%, and improved cardiac function by 30% vs. controls (p < 0.05). These benefits were associated with attenuation in DNA-oxidative damage and apoptotic markers and increased iNOS in the infarcted myocardium, higher AMPK activation in the remote myocardium, and lower myocardial MCP-1 expression. Systemically, spirulina attenuated Cox-2 expression in STEMI-activated peripheral blood mononuclear cells and enhanced TNF-α release acutely post-STEMI. Additionally, spirulina decreased weight gain progression over time (p < 0.05) without changes in lipids, glucose, liver or kidney parameters.Conclusion: A 10-day supplementation with spirulina exerts cardioprotection in a preclinical setting of STEMI by limiting cardiac damage and improving ventricular contractility through anti-oxidative, anti-inflammatory, and anti-apoptotic mechanisms.

Sepsis is a life-threatening organ dysfunction syndrome caused by host response disorders due to infection or infectious factors and is a common complication of patients with clinical trauma, burns, and infection. Resveratrol is a natural polyphenol compound that is a SIRT-1 activator with anti-inflammatory, antiviral, antibacterial, antifungal inhibitory abilities as well as cardiovascular and anti-tumor protective effects. In recent years, some scholars have applied resveratrol in animal models of sepsis and found that it has an organ protective effect and can improve the survival time and reduce the mortality of animals with sepsis. In this study, Medline (Pubmed), embase, and other databases were searched to retrieve literature published in 2021 using the keywords "resveratrol" and "sepsis," and then the potential of resveratrol for the treatment of sepsis was reviewed and prospected to provide some basis for future clinical research. [ABSTRACT FROM AUTHOR]

Sepsis is a life-threatening organ dysfunction syndrome caused by host response disorders due to infection or infectious factors and is a common complication of patients with clinical trauma, burns, and infection. Resveratrol is a natural polyphenol compound that is a SIRT-1 activator with anti-inflammatory, antiviral, antibacterial, antifungal inhibitory abilities as well as cardiovascular and anti-tumor protective effects. In recent years, some scholars have applied resveratrol in animal models of sepsis and found that it has an organ protective effect and can improve the survival time and reduce the mortality of animals with sepsis. In this study, Medline (Pubmed), embase, and other databases were searched to retrieve literature published in 2021 using the keywords “resveratrol” and “sepsis,” and then the potential of resveratrol for the treatment of sepsis was reviewed and prospected to provide some basis for future clinical research.

Epilepsy, a chronic neurological disorder affecting millions globally, is often exacerbated by neuroinflammation and oxidative stress. Existing antiepileptic drugs primarily manage symptoms, leaving the disease's progression largely unaddressed. Flavonoids, ubiquitous plant metabolites with potent anti-inflammatory and antioxidant properties, show promise in epilepsy treatment. Unlike conventional therapies, they target multiple pathophysiological processes simultaneously, offering a comprehensive approach to this complex neurological disorder. This review explores the dual role of flavonoids in mitigating neuroinflammation and reducing oxidative stress through various molecular pathways. By inhibiting key inflammatory mediators and pathways such as NF-κB, MAPK, JNK, and JAK, flavonoids offer neuronal protection. They enhance the body's natural antioxidant defenses by modulating enzyme activities, including superoxide dismutase, catalase, and glutathione peroxidase. Moreover, flavonoids influence crucial antioxidant response pathways like PI3K/AKT, Nrf2, JNK, and PKA. Despite their therapeutic promise, the low bioavailability of flavonoids poses a considerable challenge. However, cutting-edge strategies, including nanotechnology and chemical modifications, are underway to improve their bioavailability and therapeutic efficacy. These advancements support the potential of flavonoids as a valuable addition to epilepsy treatment strategies., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Zhang, Hu and Zou.)

Huolisu Oral Liquid (HLS), a well-known traditional Chinese medicine (TCM) prescription, is an over-the-counter drug that is registered and approved by the State Food and Drug Administration (Approval No. Z51020381). HLS has been widely applied in the clinical treatment of cognitive disorders and has effects on delaying aging. The antioxidant effects of HLS are closely related to its antiaging activities, but the underlying mechanisms are unclear. In this study, the potential antioxidant ingredients of HLS were screened based on serum pharmacochemistry and network pharmacology, and the potential mechanisms involved in HLS antioxidant effects were preliminarily explored. Further, the antioxidant effects of HLS were verified by in vivo and in vitro experiments. The results showed that potential antioxidant ingredients could affect the toxic advanced glycation end products-receptor for advanced glycation end products (TAGE-RAGE) signaling, mitogen-activated protein kinase (MAPK) signaling, interleukin (IL)-17 signaling, tumor necrosis factor (TNF) signaling, toll-like receptors (TLRs), cyclic adenosine monophosphate (cAMP) signaling, hypoxia-inducible factor (HIF)-1 signaling, and other related pathways by regulating GAPDH, AKT1, TP53, MAPK1, JUN, and other associated targets. Thus, HLS may reduce inflammation, control the release of inflammatory cytokines, and regulate mitochondrial autophagy and metabolic abnormalities to ultimately play an antioxidant role. This is the first study attempting to construct a multilevel network of "HLS-antioxidant targets" based on serum pharmacochemistry and network pharmacology to explore the relationship between HLS and antioxidation and the molecular mechanisms of antioxidation combined with bioinformatics functional analysis and lays a foundation for further elucidating the antioxidant mechanisms of HLS. [ABSTRACT FROM AUTHOR]

Huolisu Oral Liquid (HLS), a well-known traditional Chinese medicine (TCM) prescription, is an over-the-counter drug that is registered and approved by the State Food and Drug Administration (Approval No. Z51020381). HLS has been widely applied in the clinical treatment of cognitive disorders and has effects on delaying aging. The antioxidant effects of HLS are closely related to its antiaging activities, but the underlying mechanisms are unclear. In this study, the potential antioxidant ingredients of HLS were screened based on serum pharmacochemistry and network pharmacology, and the potential mechanisms involved in HLS antioxidant effects were preliminarily explored. Further, the antioxidant effects of HLS were verified by in vivo and in vitro experiments. The results showed that potential antioxidant ingredients could affect the toxic advanced glycation end products-receptor for advanced glycation end products (TAGE-RAGE) signaling, mitogen-activated protein kinase (MAPK) signaling, interleukin (IL)-17 signaling, tumor necrosis factor (TNF) signaling, toll-like receptors (TLRs), cyclic adenosine monophosphate (cAMP) signaling, hypoxia-inducible factor (HIF)-1 signaling, and other related pathways by regulating GAPDH, AKT1, TP53, MAPK1, JUN, and other associated targets. Thus, HLS may reduce inflammation, control the release of inflammatory cytokines, and regulate mitochondrial autophagy and metabolic abnormalities to ultimately play an antioxidant role. This is the first study attempting to construct a multilevel network of “HLS-antioxidant targets” based on serum pharmacochemistry and network pharmacology to explore the relationship between HLS and antioxidation and the molecular mechanisms of antioxidation combined with bioinformatics functional analysis and lays a foundation for further elucidating the antioxidant mechanisms of HLS.

Coronary heart disease (CHD) is the most common clinical manifestation of cardiovascular disease. It is characterized by myocardial ischemia, which is caused by coronary atherosclerosis. CHD is a significant global health problem with increasing prevalence every year because of significant changes in the lifestyles and diets. Ginseng is a traditional Chinese medicinal herb that has been used in food preparations and traditional medicine for several centuries. Several studies have demonstrated that ginseng improved cardiac function by normalizing blood glucose levels and decreasing blood pressure, oxidative stress, platelet aggregation, and lipid dysregulation in vivo . This review describes the current understanding of the mechanisms by which ginseng alleviates CHD, and provides a reference for the clinical development and application of ginseng as an alternative therapy for CHD., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Tang, Zhao, Li and Hou.)

Although Panax notoginseng (PN) roots in raw and steamed forms were historically supposed to be different in the efficacies, the raw materials and steamed ones were often undifferentiated in the use and market circulation, which might bring unstable curative effects or even adverse reactions. To uncover chemical constituents responsible to different activities of raw and steamed PN, chemometrics analyses including partial least squares regression (PLSR) and multi-linear regression analysis (MLRA) were used to establish the relationships between the chromatographic fingerprints and activities of PN samples. Chemical fingerprints of PN were determined by HPLC. Anticoagulant and antioxidant activities were evaluated by the thromboplastin inhibiting test and hydroxyl radical scavenging assay, respectively. Results showed that there was a significant difference in the chemical composition between raw and steamed PN, which could be discriminated by principle component analysis according to different steaming temperatures. Compared with the steamed PN, raw PN exhibited stronger anticoagulation and weaker antioxidation. By chemometrics analyses, notoginsenoside R1, ginsenosides Rg1, Re, Rb1, and Rd were found to be the major active constituents of raw PN, whereas ginsenosides Rh1, Rk3, Rh4, and 20(R)-Rg3 had the key role in the activities of steamed PN, which could be used as new markers for the quality control (QC) of steamed PN.

Chickpea (Cicer arietinum) is a legume of the family Fabaceae, subfamily Faboideae. In Egypt, chickpea seeds are usually consumed at raw green and tender stage, or in the form of mature dry seeds. In our previous study, ‘Giza 1’ seeds exhibited stronger antioxidant activity and high total phenol content than those from other Egyptian cultivars. In order to assess the biological potential of ‘Giza 1’ seeds in vivo, the extraction procedure was reproduced here. The extract was standardized using liquid chromatography (LC) coupled to diode array detector (DAD) and tandem mass spectrometry (MS/MS) to evaluate their hepatoprotective effect on CCl4-induced hepatotoxicity in rats and acute toxicity. Administration of the extract to rats in doses up to 2 g/Kg) did not cause any mortalities or observable signs of toxicity. Further, the plant extract showed a strong hepatoprotective activity based on assessing serum alanine aminotranferase, aspartate aminotranferase, and alkaline phosphatase and levels of albumen, globulin, total protein, total cholesterol, high density lipoprotein, triglycerides, and low density lipoprotein. The antioxidative activity was evaluated by assessing hepatic catalase and superoxide dismutase activity as well as reduced glutathione, and malondialdehyde levels. Additionally, anti-inflammatory activity was observed as the extract significantly lowered the hepatic tumor necrosis factor α content. Histopathological examination of liver tissues indicated that the extract-treated animals showed almost normal hepatic architecture with fewer pathological changes. In conclusion, the current results suggest that the chickpea extract possesses an excellent safety profile with very low acute toxicity. Also, it exhibits a significant hepatoprotective effect against CCl4-induced liver injury in rats. This can be attributed, at least partly, to the antioxidant and anti-inflammatory activity of the isoflavones and phenolic acids content of the extract.

Chickpea (Cicer arietinum) is a legume of the family Fabaceae, subfamily Faboideae. In Egypt, chickpea seeds are usually consumed at raw green and tender stage, or in the form of mature dry seeds. In our previous study, 'Giza 1' seeds exhibited stronger antioxidant activity and higher total phenol content than those from other Egyptian cultivars. In order to assess the biological potential of 'Giza 1' seeds in vivo, the extraction procedure was reproduced here. The extract was standardized using liquid chromatography coupled to diode array detector and tandem mass spectrometry (MS/MS) to evaluate their hepatoprotective effect on carbon tetrachloride (CCl4)-induced hepatotoxicity in rats and acute toxicity. Administration of the extract to rats in doses up to 2 g/Kg) did not cause any mortalities or observable signs of toxicity. Further, the plant extract showed a strong hepatoprotective activity based on assessing serum alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase and levels of albumen, globulin, total protein, total cholesterol, high density lipoprotein, triglycerides, and low density lipoprotein. The antioxidative activity was evaluated by assessing hepatic catalase and superoxide dismutase activity as well as reduced glutathione, and malondialdehyde levels. Additionally, anti-inflammatory activity was observed as the extract significantly lowered the hepatic tumor necrosis factor α content. Histopathological examination of liver tissues indicated that the extract-treated animals showed almost normal hepatic architecture with fewer pathological changes. In conclusion, the current results suggest that the chickpea extract possesses an excellent safety profile with very low acute toxicity. Also, it exhibits a significant hepatoprotective effect against CCl4-induced liver injury in rats. This can be attributed, at least partly, to the antioxidant and anti-inflammatory activity of the isoflavones and phenolic acids content of the extract. [ABSTRACT FROM AUTHOR]

Astaxanthin (ASX) is a kind of carotenoid widely distributed in nature, which has been shown to extremely strong antioxidative effects and significant preventive and therapeutic effects on cancer, diabetes, cardiovascular disease, etc. However, its application in the medical field is greatly limited due to its poor water solubility, unstable chemical properties and other shortcomings. In recent years, the nano-based drug delivery systems such as nanoparticles, liposomes, nanoemulsions, nanodispersions, and polymer micelles, have been used as Astaxanthin delivery carriers with great potential for clinical applications, which have been proved that they can enhance the stability and efficacy of Astaxanthin and achieve targeted delivery of Astaxanthin. Herein, based on the pharmacological effects of Astaxanthin, we reviewed the characteristics of various drug delivery carriers, which is of great significance for improving the bioavailability of Astaxanthin., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Chen, Wang, Feng and Xuan.)

Although Panax notoginseng (PN) roots in raw and steamed forms were historically supposed to be different in the efficacies, the raw materials and steamed ones were often undifferentiated in the use and market circulation, which might bring unstable curative effects or even adverse reactions. To uncover chemical constituents responsible to different activities of raw and steamed PN, chemometrics analyses including partial least squares regression (PLSR) and multi-linear regression analysis (MLRA) were used to establish the relationships between the chromatographic fingerprints and activities of PN samples. Chemical fingerprints of PN were determined by HPLC. Anticoagulant and antioxidant activities were evaluated by the thromboplastin inhibiting test and hydroxyl radical scavenging assay, respectively. Results showed that there was a significant difference in the chemical composition between raw and steamed PN, which could be discriminated by principle component analysis according to different steaming temperatures. Compared with the steamed PN, raw PN exhibited stronger anticoagulation and weaker antioxidation. By chemometrics analyses, notoginsenoside R 1 , ginsenosides Rg 1 , Re, Rb 1 , and Rd were found to be the major active constituents of raw PN, whereas ginsenosides Rh 1 , Rk 3 , Rh 4 , and 20( R )-Rg 3 had the key role in the activities of steamed PN, which could be used as new markers for the quality control (QC) of steamed PN.