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All issues Volume 31 / No 3 (June 2026) Wuhan Univ. J. Nat. Sci., 31 3 (2026) 305-310 Full HTML
Open Access
Issue
Wuhan Univ. J. Nat. Sci.
Volume 31, Number 3, June 2026
Page(s) 305 - 310
DOI https://doi.org/10.1051/wujns/2026313305
Published online 24 June 2026

© Wuhan University 2026

Licence Creative CommonsThis is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

0 Introduction

High-altitude and arid-region ecotype of Brassica rapa L. (hereinafter referred to as HAD-Br) is a dicotyledonous plant belonging to the genus Brassica (family Brassicaceae). In the Qinghai-Xizang Plateau and the Tarim Basin of Xinjiang, HAD-Br not only serves as an important local food source but also plays a key role in traditional Tibetan and Uyghur medicine, where it has long been used to treat respiratory infections, alleviate high-altitude hypoxia, and relieve fatigue[1-3].

The bioactive components and modern pharmacological mechanisms of HAD-Br sourced from these regions have recently garnered widespread attention. Emerging evidence indicates that extreme ecological stressors—including high-altitude cold and intense ultraviolet radiation on the Qinghai-Xizang Plateau, alongside severe drought and dramatic diurnal temperature shifts in Xinjiang—significantly drive the synthesis and accumulation of secondary metabolites[4]. These include polysaccharides, specific phenolic compounds, and glucosinolates, which collectively provide the crucial material basis for the plant's multitarget biological effects.

A substantial body of in vitro and in vivo research has confirmed that HAD-Br extracts and isolated bioactive compounds from these specific ecotypes exhibit robust therapeutic efficacy across various pathological models. Notably, they demonstrate outstanding potential in mitigating high-altitude hypoxia, ameliorating neurodegenerative conditions, and conferring hepatoprotective effects[3,5-6]. Furthermore, significant progress has been made in immune microenvironment regulation, antitumor activity, and prebiotic-mediated remodeling of the gut microbiota[2,7-9]. Based on these advancements, this review systematically summarizes the major chemical constituents of endemic HAD-Br from the Qinghai-Xizang and Xinjiang regions, elucidating its core pharmacological effects and underlying molecular mechanisms. Ultimately, this synthesis aims to provide a robust scientific foundation for the further valorization of this characteristic medicinal and edible plant from alpine and arid regions.

1 Bioactive Ingredients of HAD-Br

HAD-Br contains a diverse array of bioactive compounds, including polysaccharides, phenolic compounds, glucosinolates, and other secondary metabolites (e.g., organic acids and terpenoids). The profile and content of these compounds vary depending on geographical origin. Notably, specific ecotypes cultivated in the Xinjiang region and the Qinghai-Xizang Plateau demonstrate a markedly enriched accumulation of these bioactive components. This phytochemical upregulation serves as a critical adaptive response to the severe local abiotic stresses, including high-altitude radiation, extreme thermal fluctuations, and prolonged drought.

1.1 Polysaccharides

Polysaccharides are among the most abundant and extensively studied classes of bioactive macromolecules in HAD-Br. To date, various polysaccharide fractions (e.g., BRCPe, BRAP, and BRLPP) have been isolated and characterized[9]. Structural analyses reveal that these polysaccharides are predominantly heteropolysaccharides, with molecular weights ranging from 5 kDa to over 800 kDa[1,10-12]. Their monosaccharide compositions vary considerably: some fractions (e.g., subfractions BRNP-1 and BRNP-2, as well as BRLPP) are primarily composed of glucose, whereas others contain varying proportions of arabinose, galactose, rhamnose, and galacturonic acid[1,6,10,13]. For example, a subfraction designated BRP-1-1 has been characterized as a glucose-rich polysaccharide (94.04% glucose) featuring a (1→4)-α-D-Glcp backbone with branching points at the O-6 position[14]. Conversely, BRAP1-1 (a subfraction derived from BRAP) has been identified as a complex heteropolysaccharide containing β-glycosidic linkages, composed of fucose, rhamnose, arabinose, galactose, and galacturonic acid[13]. The structural diversity of these polysaccharides, including differences in molecular weight, degree of branching, and uronic acid content, directly influences their physicochemical properties and biological activities.

1.2 Phenolic Compounds

HAD-Br is rich in diverse phenolic compounds, which are primary contributors to its robust antioxidant capacity. The extreme high-altitude environmental stress acts as a major catalyst for the accumulation of flavonoids (such as quercetin, apigenin, and kaempferol) and specific phenolic acids, thereby reinforcing the plant's defense mechanisms. Interestingly, while typical Brassicaceae phenolics dominate, recent integrated UHPLC-MS and network pharmacology analyses have also annotated unconventional metabolites, including gingerol analogues (6-paradol, 6-gingerol, and 6-shogaol), in ecotypes native to the Qinghai-Xizang Plateau[4]. Together, these complex phenolic networks exhibit considerable geroprotective, neuroprotective, and anti-inflammatory activities.

1.3 Glucosinolates

As characteristic constituents of Brassicaceae plants, glucosinolates are abundantly present in HAD-Br. Upon hydrolysis by the endogenous enzyme myrosinase, glucosinolates generate isothiocyanates, which exhibit notable chemopreventive and anti-inflammatory activities. HAD-Br glucosinolates have been isolated and purified, and their stability and sustained-release properties have been improved through encapsulation in zein/chitosan nanoparticles[15].

1.4 Other Bioactive Constituents

In addition to the major classes described above, HAD-Br also contains organic acids, amino acids, and sugar derivatives. Furthermore, endophytic fungi isolated from HAD-Br, such as strain pr10, have been shown to produce antitumor metabolites, including trehalose and other sugar derivatives, suggesting that microorganisms may contribute to the overall bioactive profile of HAD-Br[16].

2 Pharmacological Properties and Therapeutic Potential of HAD-Br

The diverse bioactive constituents of HAD-Br underpin its broad-spectrum pharmacological effects. Preclinical studies using diverse in vitro and in vivo models have substantiated its multifaceted therapeutic potential[3,6-7]. Specifically, these extracts exhibit robust efficacies in neuroprotection, fatigue amelioration, immunomodulation, tumor suppression, and hepatoprotection, while also regulating gut microbiota homeostasis.

2.1 Neuroprotective Effects

Neuroprotection is one of the most extensively investigated pharmacological properties of HAD-Br. Multiple studies[3,17,22] have demonstrated that HAD-Br extracts and its active constituents exert protective effects against cerebral ischemia, hypoxia, and sleep deprivation-induced cognitive dysfunction. In a mouse model of transient middle cerebral artery occlusion/reperfusion, aqueous extract of HAD-Br significantly reduced cerebral infarct volume and improved behavioral outcomes[18]. Mechanistically, this effect is primarily mediated by activation of the PI3K/Akt/mTOR signaling pathway, thereby attenuating oxidative stress, reducing neuronal apoptosis, and preserving mitochondrial function[3,17-18]. Similarly, a bioactive monomer isolated from Tibetan HAD-Br protected HT22 cells against oxygen-glucose deprivation/reoxygenation injury via the same pathway[3]. In a sleep-deprived mouse model, an extract of HAD-Br ameliorated cognitive deficits by inhibiting neuroinflammation and restoring hippocampal mitochondrial energy metabolism via the AMPK/PPAR-γ pathway[19]. Additionally, a bioactive compound BREE-Ea from turnip has shown therapeutic potential in Alzheimer's disease models by reducing Aβ deposition and tau phosphorylation[5].

2.2 Anti-Aging Effects

The anti-aging potential of HAD-Br has been evaluated using the Caenorhabditis elegans model. Extracts from turnip originating from the Qinghai-Xizang Plateau, which exhibit higher phenolic content, significantly extended the healthspan of nematodes, enhanced locomotor capacity, and downregulated the expression of senescence markers[4]. Network pharmacology analysis identified 6-paradol, 6-gingerol, and 6-shogaol as key contributors to the anti-aging regulatory network, with 6-shogaol alone extending healthspan by 28.4% and activating longevity pathways[4].

2.3 Anti-Fatigue Effects and Enhancement of Exercise Performance

HAD-Br extracts and polysaccharides have demonstrated pronounced anti-fatigue effects in forced swimming tests and models of chronic exercise-induced fatigue. Treatment with turnip extract reduced serum levels of blood lactate, blood urea nitrogen, and creatine kinase, while increasing glycogen storage and ATP content[12,20]. The AMPK/PGC-1α/TFAM signaling pathway was identified as a key mediator of these effects, regulating energy metabolism in skeletal muscle[15,21]. In addition, HAD-Br extract alleviated exercise-induced gut dysbiosis by enriching beneficial genera such as Lactobacillus and Alloprevotella while suppressing pathogenic bacteria such as Staphylococcus[15]. The anti-fatigue activity is also linked to modulation of immune function and oxidative stress, as shown by Brassica rapa L. extract (BE) treatment in forced swimming mice[2,20].

2.4 Immunomodulatory Activity

HAD-Br polysaccharides exhibit potent immunomodulatory activity. In RAW264.7 macrophages, HAD-Br polysaccharides stimulated cell proliferation, induced nitric oxide release, and promoted secretion of the cytokines IL-6 and TNF-α[10]. In a cyclophosphamide-induced immunosuppressed mouse model, HAD-Br polysaccharides restored immune organ indexes, enhanced immune cell activity, and increased serum levels of immunoglobulins and cytokines, in part through modulation of the TLR4/NF-κB signaling pathway[22]. Furthermore, turnip polysaccharides have been shown to polarize macrophages from the M2 to the M1 phenotype, thereby contributing to their antitumor effects[23]. Network pharmacology and metabolomics also revealed that BE regulates energy metabolism and inflammation via Nrf2/HO-1 and AMPK pathways, and reverses M1 polarization in RAW264.7 cells[2].

2.5 Antitumor Activity

The antitumor potential of HAD-Br has been demonstrated in both in vitro and in vivo models. The petroleum ether extract (BRPS) inhibited the proliferation of human lung adenocarcinoma A549 cells and mouse Lewis lung carcinoma (LLC) cells, inducing G2/M phase arrest and mitochondria-dependent apoptosis, as evidenced by an increased Bax/Bcl-2 ratio, cytochrome c release, and activation of caspase-9 and caspase-3. BRPS also enhanced antitumor immunity by increasing the proportions of B cells, CD4⁺ T cells, and CD8⁺ T cells in the spleen[8]. When combined with cisplatin, HAD-Br polysaccharides (BRCPe) synergistically suppressed the growth of hepatocellular carcinoma while mitigating cisplatin-induced side effects, including weight loss and immune deficiency[9]. Moreover, turnip polysaccharides (BP) have been shown to inhibit Lewis lung cancer growth by reducing inflammation, preserving intestinal barrier, and modulating gut microbiota (e.g., Blautia, Bifidobacterium)[24]. Additionally, Brassica rapa polysaccharide (BRP) induces M1-like macrophage polarization via STAT signaling, contributing to tumor suppression[23].

2.6 Hepatoprotective Effects

Multiple studies have confirmed the hepatoprotective effects of HAD-Br against chemically induced liver injury. HAD-Br polysaccharides ameliorated CCl4-induced acute liver injury by reducing serum transaminase (ALT and AST) levels, suppressing oxidative stress, and inhibiting inflammatory responses through downregulation of the JAK2/STAT3 signaling pathway[25]. Sinapine thiocyanate, a major component in HAD-Br seeds, also exhibited dose-dependent hepatoprotective effects[26]. In an ethanol-induced HepG2 cell model of alcoholic liver injury, turnip extract alleviated cell injury via activation of the PI3K/Akt pathway[27]. Furthermore, a purified polysaccharide BRLPP from turnip demonstrated hepatoprotection in a zebrafish alcoholic liver disease (ALD) model by reducing ALT/AST and oxidative stress markers[6].

2.7 Modulation of Gut Microbiota and Protection of Intestinal Barrier Function

Accumulating evidence supports the prebiotic-like effects of turnip polysaccharides. In vitro fermentation and in vivo studies have shown that HAD-Br polysaccharides are not degraded during gastrointestinal digestion but are fermented by gut microbiota, leading to increased production of short-chain fatty acids and modulation of microbial composition[7,13,28]. In a hypobaric hypoxia-induced intestinal injury model, turnip polysaccharides restored intestinal barrier function by upregulating the expression of tight junction proteins (claudin-1, occludin, ZO-1) and enriched beneficial bacteria such as Akkermansia muciniphila and Lactobacillus, while reducing pathogenic taxa[28-29]. These effects were associated with enhanced antioxidant capacity and reduced inflammation. In diabetic and tumor-bearing mouse models, turnip polysaccharides similarly reshaped the gut microbiota, promoting the enrichment of short-chain fatty acid-producing genera and suppressing lipopolysaccharide- producing bacteria, thereby contributing to the maintenance of metabolic and immune homeostasis[24,30]. A synbiotic fermented whey beverage containing turnip crude polysaccharides also activated AMPK signaling and increased berberine/nicotinic acid levels to alleviate hypoxia-induced intestinal damage[29].

2.8 Pulmonary Protective Effects

A study extracted and purified a polysaccharide (designated BRP) from HAD-Br and found that in a bleomycin-induced pulmonary fibrosis model, BRP alleviated fibrotic pathology by modulating inflammatory, epithelial-mesenchymal transition, and fibrotic pathways[14]. BRP treatment downregulated TGF-β and α-SMA expression, suppressed NF-κB and NLRP3 activation, and reduced collagen deposition, highlighting its therapeutic potential against respiratory diseases[14].

3 Conclusion

Over the past five years, significant progress has been made in understanding the chemical diversity and pharmacological profile of HAD-Br. Polysaccharides, phenolic compounds, and glucosinolates constitute its major bioactive constituents, underpinning its multifaceted efficacy in neuroprotection, anti-aging, anti-fatigue, immunomodulation, antitumor activity, hepatoprotection, and gut microbiota regulation[2,4-8,29]. Mechanistically, HAD-Br-derived bioactive components act through multiple signaling pathways, including PI3K/Akt, AMPK, NF-κB, and JAK2/STAT3, reflecting the multi-target nature of its therapeutic effects[15,18,21,25].

Despite these advances, several challenges remain. First, the precise chemical structures of many bioactive polysaccharides and their structure-activity relationships warrant further elucidation. Second, although network pharmacology and metabolomics have provided valuable insights into multi-target mechanisms, these findings still require validation through targeted genetic or pharmacological approaches. Third, the bioavailability and in vivo metabolic fate of key constituents, particularly following oral administration, remain underexplored. Finally, current research has largely focused on crude extracts or mixed fractions, and systematic pharmacokinetic studies on individual bioactive components are still insufficient, which limits their precise translation into standardized functional foods or dietary supplements.

In summary, the available evidence strongly indicates that HAD-Br, as an ancient medicinal and edible plant, holds great promise for the development of functional food ingredients and therapeutic agents. Future research should aim to integrate chemical characterization, mechanistic studies, and clinical validation to fully realize the value of this traditional resource in promoting human health.

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