Protective effect of Curcuma longa L. leaves and pseudostems extract against 1-chloro-2,4-dinitrobenzene-induced...

The perennial herbaceous plant, Curcuma longa L. (turmeric) is primarily grown and harvested for pharmacological purposes in China, Korea, and various tropical regions in South Asia. Turmeric has been used for centuries as an indigenous medicine. In particular, Ayurveda has been extensively used to treat, prevent, and manage multiple illnesses, including inflammation, allergies, arthritis, cancer, diabetes, diarrhea, psoriasis, and digestive issues. Importantly, various studies have confirmed the presence of numerous active compounds with health-enhancing biological properties in turmeric leaves and pseudostems.

Atopic dermatitis (AD) is a long-lasting inflammatory disorder that is associated with abnormalities in the immune system, such as T-helper (Th) cell dysregulation, elevated immunoglobulin (Ig) levels, inflammatory cell infiltration, and skin barrier damage. This study aimed to explore the therapeutic effects of turmeric leaves and pseudostems (CLHW) extract against AD in a BALB/c mouse disease model established using 1-chloro-2,4-dinitrobenzene (DNCB).

AD-like symptoms were induced by topically applying DNCB to the dorsal skin of the mice, which were monitored over five weeks. Fourteen days after induction, the mice were randomly divided into different groups, and the treatment groups received daily oral gavage of CLHW for three weeks. Throughout the monitoring period, we assessed AD-like symptoms, including skin severity score, transepidermal water loss (TEWL), and scratching behavior of the mice. After measuring the body weight and ear thickness, the mice were euthanized. Furthermore, serum Ig and cytokine production levels were measured. Finally, the degrees of spleen and lymph node enlargement were evaluated, and the tissues were used for histopathological and molecular analyses.

CLHW improved AD-like symptoms, including skin severity score, TEWL, scratching frequency, and ear thickness in DNCB-induced AD mice. Additionally, serum levels of IgE, IgG₁, and IgG_2a, along with various inflammatory cytokines (interleukin [IL]-4, IL-5, and IL-13) and chemokines (Eotaxin and RANTES), were significantly reduced in CLHW-treated mice. CLHW decreased inflammatory cell infiltration and mast cell degranulation while downregulating mRNA expression levels of AD-related innate cytokines (thymic stromal lymphopoietin [TSLP], IL-25, IL-33), inflammatory cytokines (IL-4, IL-10, IL-13), and chemokines (thymus and activation-regulated chemokine [TARC], macrophage-derived chemokine [MDC]) in the dorsal skin. Furthermore, CLHW reduced spleen and lymph node enlargement and downregulated mRNA expression levels of inflammatory cytokines in these tissues in a dose-dependent manner.

The results demonstrated that CLHW can effectively suppress DNCB-induced AD-like symptoms by reducing the skin severity score, TEWL, scratching, ear thickness, serum Ig levels, inflammatory cell infiltration, and degranulation of mast cells, as well as the enlargement of the spleen and lymph nodes. Our findings highlight the ethnopharmacological potential of CLHW for treating abnormal immune responses associated with AD.