Non-Bovine Milk as Functional Foods with Focus on Their Antioxidant and Anti-Inflammatory Bioactivities

Abstract

The growing interest in functional foods has directed scientific attention toward alternative milk sources, particularly camel and donkey milk, which have been traditionally consumed for their purported health benefits across diverse cultures. These milk sources possess unique nutritional profiles and bioactive compositions that differ substantially from conventional bovine milk. This review examines the current scientific understanding of the anti-inflammatory and antioxidant bioactivities of camel and donkey milk, exploring their bioactive constituents and therapeutic potential. Camel and donkey milk demonstrate notable antioxidant and anti-inflammatory properties that may exceed those of conventional milk sources. Key bioactive compounds include lactoferrin, lysozyme, immunoglobulins, bioactive peptides, vitamins C and E, and polyunsaturated fatty acids. Mechanistic studies reveal that milk from donkeys and camels suppresses inflammatory pathways through NF-κB inhibition, cytokine modulation (reducing IL-6, IL-1β, and TNF-α while enhancing IL-10), and antioxidant pathway activation via Nrf2-ARE signaling. Donkey milk exhibits particularly high lysozyme content and demonstrates significant immunomodulatory effects, while camel milk shows remarkable therapeutic potential in diabetes management, nephroprotection, and hepatoprotection. Preclinical studies demonstrate efficacy in treating oxidative stress-related disorders, inflammatory conditions, metabolic dysfunction, and tissue injury models. Altogether, the published data show that camel and donkey milk represent promising functional foods with significant antioxidant and anti-inflammatory bioactivities mediated through multiple molecular pathways. Their unique bioactive profiles offer therapeutic potential for various health conditions, warranting further clinical investigation and development as nutraceutical interventions.

Keywords: antioxidant and anti-inflammatory activities; bioactive compounds; camel milk; donkey milk; functional foods; therapeutic potential.

Figure 1

Antioxidant and anti-inflammatory potential of camel and donkey milk. This figure illustrates the comprehensive protective mechanism by which camel and donkey milk components counteract cellular damage caused by oxidative stress. Environmental stressors, pathogens, and toxicants enter the cell through toll-like receptor 4 (TLR4) and activate myeloid differentiation factor 88 (MyD88) pathway, leading to the generation of reactive oxygen species (ROS). ROS production results in mitochondrial damage and triggers oxidative stress, which normally would lead to cellular dysfunction and apoptosis. Camel and donkey milk components intervene in this cascade by modulating key signaling pathways—specifically inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling to reduce inflammation and regulating apoptotic signaling to promote anti-apoptotic responses. The activation of nuclear factor erythroid-2 related factor 2 (Nrf2) signaling leads to enhanced antioxidant responses, which suppress oxidative stress and consequent damage.

Figure 2

The molecular mechanism of donkey and camel milk to combat inflammation. The figure illustrates that camel and donkey milk work through multiple mechanisms to inhibit the NF-κB inflammatory pathway, including regulation of the HMGB1/TLR4/NF-κB/MyD88 signaling pathway and downregulation of NF-κB pathway activation by decreasing protein expression of activated NF-κBp65, p-NF-κBp65, and p-IκBα proteins. In addition, the figure demonstrates that camel milk is particularly effective as an anti-inflammatory agent—by targeting the phosphorylation step that is essential for MAPK activation, it can simultaneously shut down multiple pro-inflammatory pathways (ERK, p38, and JNK) that would otherwise lead to production of inflammatory mediators’ land matrix metalloproteinases.

Figure 3

Molecular mechanism of prevention of hepatic inflammation and injury by camel milk. This figure illustrates how camel whey protein protects hepatocytes by blocking inflammation and apoptosis pathways. The diagram shows a liver cell where HMGB1 molecules normally bind to RAGE receptors, activating the NLRP3 inflammasome complex. This activation triggers two harmful responses: Caspase-1 converts Pro-IL-1β to mature IL-1β (promoting inflammation), and Caspase-3 activation leads to cell death. However, camel whey protein intervenes by inhibiting HMGB1 activity, as shown by the red inhibition arrow and X marks throughout the pathway. This blockade prevents both inflammatory cytokine production and apoptosis, demonstrating camel whey protein’s potential as a liver-protective therapeutic agent that simultaneously targets multiple pathological processes. The figure is adopted based on findings of Du et al. [157,158,159].

Figure 4

Camel milk—health properties and potential therapeutic applications. This figure presents a clear distinction between established health properties of camel milk (left panel) and potential therapeutic applications under investigation (right panel). The central positioning emphasizes camel milk as the source of both documented properties and research interests while avoiding implications of direct treatment recommendations. Important Note: The therapeutic applications shown represent areas of ongoing research and should not be interpreted as medical recommendations. Further clinical studies are needed to establish efficacy and safety profiles.