The current study was designed to evaluate the 2-hydroxybenzohydrazide (HBH) as a drug having efficacy against pyrexia, inflammation, and nociception. Besides, the therapeutic effects of HBH on oxidative stress and C-reactive proteins were also evaluated. The pharmacological studies on HBH (20–60 mg/kg) were conducted using nociception, inflammation, and pyrexia standard models. Naloxone antagonism was performed to assess the possible involvement of opioidergic mechanisms. The antioxidant study was conducted on ABTS and DPPH assays using gallic acid as a standard. Moreover, the binding capability of HBH with enzymes cyclooxygenase-I/II (COX-I/II) was determined using molecular modeling analysis. The findings indicated that the HBH dose-dependently inhibited pain, inflammation, and pyrexia. The HBH has significant anti-nociceptive and anti-inflammatory activities at 60 mg/kg (^***p < 0.001), similar to the lower doses of diclofenac sodium (50 mg/kg) and tramadol (30 mg/kg). The HBH at 60 mg/kg reduced pyrexia as paracetamol (150 mg/kg). The HBH at 20–60 mg/kg doses declined the plasma C-reactive protein concentration. The mechanistic studies showed that the anti-nociceptive effect of HBH was antagonized by naloxone, indicating that the opioidergic mechanisms are involved. Furthermore, computational studies showed that the HBH exhibited an affinity for COX-I/II target receptors. The HBH significantly inhibited ABTS and DPPH radicals (IC₅₀ = 33.81 and 26.74 μg/ml). These results proposed that the HBH has significant antipyretic, anti-inflammatory, and anti-nociceptive activities involving opioidergic mechanism.

目前的研究旨在评估 2-羟基苯甲酰肼 (HBH) 作为一种对发热、炎症和伤害感受有效的药物。此外，还评估了 HBH 对氧化应激和 C 反应蛋白的治疗作用。HBH（20-60 mg/kg）的药理学研究是使用伤害感受、炎症和发热标准模型进行的。进行纳洛酮拮抗作用以评估阿片受体机制的可能参与。使用没食子酸作为标准品，通过 ABTS 和 DPPH 测定进行抗氧化剂研究。此外，使用分子模型分析确定了 HBH 与环氧合酶-I/II (COX-I/II) 的结合能力。研究结果表明，HBH 剂量依赖性地抑制疼痛、炎症和发热。^{60 mg/kg ( ***} p < 0.001)的 HBH 具有显着的抗伤害和抗炎活性 ，类似于较低剂量的双氯芬酸钠 (50 mg/kg) 和曲马多 (30 mg/kg)。60 mg/kg 的 HBH 以扑热息痛 (150 mg/kg) 的形式减少发热。20-60 mg/kg 剂量的 HBH 降低了血浆 C 反应蛋白浓度。机制研究表明，HBH 的抗伤害作用被纳洛酮拮抗，表明涉及阿片受体机制。此外，计算研究表明 HBH 对 COX-I/II 靶受体表现出亲和力。HBH 显着抑制 ABTS 和 DPPH 自由基（IC ₅₀  = 33.81 和 26.74 μg/ml）。这些结果表明，HBH 具有显着的解热、抗炎和抗伤害活性，涉及阿片受体机制。