It has been well‐documented that the consumption of deep sea water (DSW) has beneficial effects on myocardial hypertrophy and cardiac apoptosis induced by hypercholesterolemia. However, the molecular mechanisms for the anti‐inflammatory effects of DSW on diabetic cardiomyopathy are still largely unclear. The main purpose of this present study was to test the hypothesis that DSW exerts anti‐inflammatory effects through the suppression of the TNF‐α‐mediated signaling pathways. IP injection of streptozotocin (STZ) at the dose of 65 mg/kg was used to establish a diabetes rat model. DSW mineral extracts that diluted in desalinated water were prepared in three different dosages and administered to the rats through gavages for 4 weeks. These dosages are DSW‐1X (equivalent to 37 mg Mg2+/kg/day), 2X (equivalent to 74 mg Mg2+/kg/day) and 3X (equivalent to 111 mg Mg2+ mg/kg/day). Immunofluorescence staining and Western blot showed that the protein expression level of TNF‐α was markedly higher in the STZ‐induced diabetic rat hearts than in the control group. Consequently, the phosphorylation levels of the TNF‐α‐modulated downstream signaling molecules and P38 mitogen‐activated protein kinases (MAPKs) were notably elevated in heart tissues of STZ‐induced diabetes. These higher phosphorylation levels subsequently upregulated NF‐κB‐modulated inflammatory mediators, such as cyclooxygenase (COX)‐II and inducible nitric oxide synthase (iNOS). However, treatment with DSW as well as MgSO4, the main mineral in DSW, significantly reversed all the alterations. These findings suggest that DSW has potential as a therapeutic agent for preventing diabetes‐related cardiovascular diseases.

中文翻译：

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深海矿物质通过抑制 TNFα 信号通路改善糖尿病引起的炎症

已有充分证据表明，深海水 (DSW) 的消耗对高胆固醇血症引起的心肌肥大和心肌细胞凋亡具有有益作用。然而，DSW对糖尿病心肌病抗炎作用的分子机制仍不清楚。本研究的主要目的是检验 DSW 通过抑制 TNF-α 介导的信号通路发挥抗炎作用的假设。腹腔注射链脲佐菌素（STZ）65 mg/kg，建立糖尿病大鼠模型。在淡化水中稀释的 DSW 矿物质提取物以三种不同的剂量制备，并通过管饲法对大鼠给药 4 周。这些剂量是 DSW-1X（相当于 37 mg Mg2+/kg/天），2X（相当于 74 mg Mg2+/kg/天）和 3X（相当于 111 mg Mg2+ mg/kg/天）。免疫荧光染色和蛋白质印迹显示，与对照组相比，STZ 诱导的糖尿病大鼠心脏中 TNF-α 的蛋白表达水平显着升高。因此，在 STZ 诱导的糖尿病心脏组织中，TNF-α 调节的下游信号分子和 P38 丝裂原活化蛋白激酶 (MAPK) 的磷酸化水平显着升高。这些较高的磷酸化水平随后上调了 NF-κB 调节的炎症介质，如环氧合酶 (COX)-II 和诱导型一氧化氮合酶 (iNOS)。然而，用 DSW 以及 DSW 中的主要矿物质 MgSO4 处理，显着逆转了所有变化。