School of Biosciences and Technology, VIT University, Vellore, Tamil Nadu, India.
J Pharm Pharmacol. 2018 Sep;70(9):1188-1199. doi: 10.1111/jphp.12946. Epub 2018 Jul 3.
In the present study, we have elaborated the anti-inflammatory mechanism of MSM through homing of CD34 stem cells towards an inflamed region by regulating hydrogen sulfide (H S) in an in vivo model of caerulein-induced acute pancreatitis (AP) and associated lung injury.
Male Swiss mice were treated with hourly intraperitoneal injections of caerulein (50 μg/kg) for 6 h. MSM (500 mg/kg) was administered intraperitoneally 1 h after the first caerulein injection (therapeutic). The serum amylase activity and myeloperoxidase (MPO) activity in lung and pancreas were measured. The levels of H S and interleukin (IL)-1β, cystathionine-γ-lyase (CSE) and CD34 expressions in pancreas and lungs were determined by RT-PCR and ELISA.
Methylsulfonylmethane significantly ameliorated pancreas and lung histopathological changes, decreased serum amylase, MPO activity and inhibited caerulein-induced IL-1β expression. Furthermore, MSM reduced caerulein-induced H S levels by alleviating the expression of CSE in pancreas and lungs and increased CD34 expression and inhibited nuclear factor (NF)-κB translocation in caerulein-induced AP and associated lung injury.
These findings indicate that MSM can effectively reduce inflammatory responses and induce the homing of CD34 cells to the injured tissues.
在本研究中,我们通过调节硫化氢(H₂S),阐述了 MSM 对卡拉胶诱导的急性胰腺炎(AP)及其相关肺损伤模型中 CD34 干细胞向炎症部位归巢的抗炎机制。
雄性瑞士小鼠接受 6 小时每小时腹腔内注射卡拉胶(50μg/kg)。在第一次卡拉胶注射后 1 小时(治疗),通过腹腔内给予 MSM(500mg/kg)。测量血清淀粉酶活性和肺、胰腺髓过氧化物酶(MPO)活性。通过 RT-PCR 和 ELISA 测定胰腺和肺中的 H₂S 以及白细胞介素(IL)-1β、胱硫醚-γ-裂解酶(CSE)和 CD34 的表达水平。
甲基磺酰甲烷显著改善了胰腺和肺的组织病理学变化,降低了血清淀粉酶、MPO 活性,并抑制了卡拉胶诱导的 IL-1β表达。此外,MSM 通过减轻胰腺和肺中 CSE 的表达降低了卡拉胶诱导的 H₂S 水平,增加了 CD34 的表达,并抑制了 NF-κB 在卡拉胶诱导的 AP 及其相关肺损伤中的易位。
这些发现表明,MSM 可以有效减轻炎症反应,并诱导 CD34 细胞归巢到受损组织。