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<p>Hyperglycemia is known to worsen lipopolysaccharide (LPS)-induced inflammatory osteolysis. However, regenerative therapy with human umbilical cord mesenchymal stem cells conditioned medium (HUCMSCs-CM) and <i>Tetragonula biroi</i> propolis nanoemulsion (PNE) may suppress inflammatory osteolysis with hyperglycemia. This study investigated how HUCMSCs-CM and PNE affected the osteoblastogenesis markers in rats with hyperglycemia and inflammatory osteolysis. Twenty-eight healthy male rats (1–2 months old) were divided into seven groups: NC (negative control), LP (100 µL LPS), HG (&gt; 230&#xa0;mg/dL), LH (100 µL LPS with hyperglycemia), LHH (LPS, hyperglycemia, and 100 µL HUCMSCs-CM), LHN (LPS, hyperglycemia, and 100 µL PNE), and LHHN (LPS, hyperglycemia), and 100 µL LPS from <i>Escherichia coli</i> was used to induce calvarial osteolysis. PNE and HUCMSCs-CM were prepared and administered subcutaneously into the calvaria. Thereafter, hyperglycemia was induced via intraperitoneal administration of 30&#xa0;mg/kg of streptozotocin for 1 week. The rats were sacrificed on day 8, and ELISA was used to measure Coll1a1, ALP, and osteopontin in the blood samples. Immunohistochemistry was employed to examine the osteoblastogenesis markers; RUNX-2, osterix, osteonectin, and osteocalcin. In the LPS-induced inflammatory osteolysis model with hyperglycemia, administration of HUCMSCs and PNE significantly increased osteoblastogenesis markers (<i>P</i> ≤ 0.05). The combination treatment showed the most pronounced effect, enhancing serum Coll1a1, ALP, and osteopontin levels, as well as RUNX-2, osterix, osteonectin, and osteocalcin expression. These findings indicate that HUCMSCs-CM and PNE synergistically promote osteoblastogenesis in hyperglycemia-aggravated inflammatory osteolysis and may represent a promising regenerative therapeutic strategy for inflammatory bone loss under compromised metabolic conditions.</p>

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Propolis nanoemulsion and mesenchymal stem cell conditioned medium promote osteoblastogenesis against lipopolysaccharide-induced osteolysis in hyperglycemic rats

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月30日

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  • Ananto Ali Alhasyimi,
  • Alexander Patera Nugraha,
  • Cendrawasih Andusyana Farmasyanti,
  • Niswati Fathmah Rosyida,
  • Hendri Susanto,
  • Muh. Ade Artasasta,
  • Putri Cahaya Situmorang,
  • Khairul Anuar Shariff

摘要

Hyperglycemia is known to worsen lipopolysaccharide (LPS)-induced inflammatory osteolysis. However, regenerative therapy with human umbilical cord mesenchymal stem cells conditioned medium (HUCMSCs-CM) and Tetragonula biroi propolis nanoemulsion (PNE) may suppress inflammatory osteolysis with hyperglycemia. This study investigated how HUCMSCs-CM and PNE affected the osteoblastogenesis markers in rats with hyperglycemia and inflammatory osteolysis. Twenty-eight healthy male rats (1–2 months old) were divided into seven groups: NC (negative control), LP (100 µL LPS), HG (> 230 mg/dL), LH (100 µL LPS with hyperglycemia), LHH (LPS, hyperglycemia, and 100 µL HUCMSCs-CM), LHN (LPS, hyperglycemia, and 100 µL PNE), and LHHN (LPS, hyperglycemia), and 100 µL LPS from Escherichia coli was used to induce calvarial osteolysis. PNE and HUCMSCs-CM were prepared and administered subcutaneously into the calvaria. Thereafter, hyperglycemia was induced via intraperitoneal administration of 30 mg/kg of streptozotocin for 1 week. The rats were sacrificed on day 8, and ELISA was used to measure Coll1a1, ALP, and osteopontin in the blood samples. Immunohistochemistry was employed to examine the osteoblastogenesis markers; RUNX-2, osterix, osteonectin, and osteocalcin. In the LPS-induced inflammatory osteolysis model with hyperglycemia, administration of HUCMSCs and PNE significantly increased osteoblastogenesis markers (P ≤ 0.05). The combination treatment showed the most pronounced effect, enhancing serum Coll1a1, ALP, and osteopontin levels, as well as RUNX-2, osterix, osteonectin, and osteocalcin expression. These findings indicate that HUCMSCs-CM and PNE synergistically promote osteoblastogenesis in hyperglycemia-aggravated inflammatory osteolysis and may represent a promising regenerative therapeutic strategy for inflammatory bone loss under compromised metabolic conditions.