Journal of ethnopharmacology · 2026
Phytotherapeutic potential of Bauhinia purpurea Linn. in hyperoxic lung injury: Insights from in vivo, network pharmacology and in silico analyses.
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Ruhinaz Kumarla Kaluva, Kalla Hari Prakash, Thimmana Lokesh V, Kanala Somasekhar Reddy, Subramani Parasuraman Aiya, Saddala Rajeswara Reddy, Panati Kalpana, Narala Venkata Ramireddy
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Bauhinia purpurea Linn., traditionally used in Southeast Asian medicine for respiratory and inflammatory conditions, exhibits potent antioxidant and anti-inflammatory properties that support its continued exploration in modern phytomedicine. However, its therapeutic potential in hyperoxia-induced acute lung injury (HALI) remains unexplored. HALI remains a significant clinical challenge, particularly in patients requiring high inspired oxygen concentrations, such as those with acute respiratory distress syndrome. The oxidative stress and inflammation associated with HALI currently lack targeted pharmacological interventions, prompting the exploration of natural products with antioxidant and anti-inflammatory properties.
OBJECTIVE: This study investigates the protective effects of the ethyl acetate extract of B. purpurea L., leaves (BPE) against HALI in a murine model.
METHODS: Mice were exposed to >95% O2 to induce HALI and treated with varying doses of BPE. Inflammatory cell infiltration, lung histopathology, alveolar-capillary barrier integrity, cytokine expression, oxidative stress markers, and antioxidant enzyme levels were assessed. LC-MS analysis, network pharmacology, and in silico docking were conducted to explore the phytochemical profile and predicted molecular interactions of BPE.
RESULTS: BPE treatment significantly reduced hyperoxia-induced leukocyte infiltration, particularly neutrophils and macrophages, into bronchoalveolar lavage (BAL) fluid. Histological analysis revealed attenuated lung injury and decreased alveolar wall thickening in BPE-treated groups. BPE also markedly lowered BAL fluid protein content and Evans blue dye extravasation, indicating reduced alveolar-capillary leakage. Gene expression analysis showed that BPE suppressed the expression of proinflammatory cytokines (IL-1β, TNFα, IL-6, and COX-2) and upregulated antioxidant genes (SOD-1, NRF-2 and NQO1). Biochemically, BPE restored catalase and superoxide dismutase levels, reduced malondialdehyde, and decreased serum nitrite concentrations. Notably, BPE restored the expression of the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ), a key regulator of anti-inflammatory responses. LC-MS profiling suggested the presence of several phytochemicals previously reported to possess antioxidant or anti-inflammatory properties, including gerberinol, pheophorbide A, rhamnetin-3-sophoroside, quercuslactone A, vernolepin, flavidulol C, and cimifugin. Network-based analyses predicted that these compounds may be associated with antioxidant and inflammatory signaling pathways relevant to HALI.
CONCLUSION: BPE confers significant protection against HALI by modulating oxidative stress, suppressing inflammatory responses, preserving alveolar integrity, and restoring PPARγ expression. Network pharmacology analysis provided supportive indications that the observed effects of B. purpurea L. extract may involve multiple phytochemical constituents.
OBJECTIVE: This study investigates the protective effects of the ethyl acetate extract of B. purpurea L., leaves (BPE) against HALI in a murine model.
METHODS: Mice were exposed to >95% O2 to induce HALI and treated with varying doses of BPE. Inflammatory cell infiltration, lung histopathology, alveolar-capillary barrier integrity, cytokine expression, oxidative stress markers, and antioxidant enzyme levels were assessed. LC-MS analysis, network pharmacology, and in silico docking were conducted to explore the phytochemical profile and predicted molecular interactions of BPE.
RESULTS: BPE treatment significantly reduced hyperoxia-induced leukocyte infiltration, particularly neutrophils and macrophages, into bronchoalveolar lavage (BAL) fluid. Histological analysis revealed attenuated lung injury and decreased alveolar wall thickening in BPE-treated groups. BPE also markedly lowered BAL fluid protein content and Evans blue dye extravasation, indicating reduced alveolar-capillary leakage. Gene expression analysis showed that BPE suppressed the expression of proinflammatory cytokines (IL-1β, TNFα, IL-6, and COX-2) and upregulated antioxidant genes (SOD-1, NRF-2 and NQO1). Biochemically, BPE restored catalase and superoxide dismutase levels, reduced malondialdehyde, and decreased serum nitrite concentrations. Notably, BPE restored the expression of the nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ), a key regulator of anti-inflammatory responses. LC-MS profiling suggested the presence of several phytochemicals previously reported to possess antioxidant or anti-inflammatory properties, including gerberinol, pheophorbide A, rhamnetin-3-sophoroside, quercuslactone A, vernolepin, flavidulol C, and cimifugin. Network-based analyses predicted that these compounds may be associated with antioxidant and inflammatory signaling pathways relevant to HALI.
CONCLUSION: BPE confers significant protection against HALI by modulating oxidative stress, suppressing inflammatory responses, preserving alveolar integrity, and restoring PPARγ expression. Network pharmacology analysis provided supportive indications that the observed effects of B. purpurea L. extract may involve multiple phytochemical constituents.