Fig. 1: Sp promotes redox-balance and cell survivability under oxidative stress and mitochondrial dysfunction.

a The ROS scavenging property of Sp was tested by exposing HeLa cells to 10 µM 3-AT to generate intrinsic oxidative radicals, followed by 250 µM Sp treatment for 15 min and staining with DCFDA. 50 µM BSO was used to deplete cellular glutathione. Mean DCFDA-fluorescence intensity (MFI) is represented as fold change over untreated samples. Data depicts mean ± s.e.m. n = 3, **P (t-test) <0.001. b The protection of the stressed cells from ROS induced cell death by 250 µM Sp treatment (for 15 min), was monitored through MTT assay and represented as mean ± s.e.m.; n = 8, ***P (t-test) <0.0001. c, d Mitochondrial dysfunction and oxidative stress was generated by exposing SHSY-5Y cells to 1 mM MPP⁺ for 24 h. The cells were then treated with 250 µM Sp for 15 min, stained by DCFDA (c) or MitoSOX (d) and MFI was represented as fold change over untreated cells. Bars show mean ± s.e.m. n = 3, **P (t-test) <0.001. e SHSY-5Y cells were subjected to treatment regimen as mentioned in (c) and the viability of cells were measured through MTT assay and depicted as mean ± s.e.m.; n = 8, ***P (t-test) <0.0001. f Sp reduces neuronal ROS in Drosophila. Relative fluorescence intensities (FI) of genetically expressing roGFP (redox-sensitive GFP) in fly brains depleted for Catalase or Glutathione peroxidase, untreated or treated with 2.5 mM Sp, compared to untreated wild-type controls. Bars represent mean ± s.e.m.; n = 10, **P (t-test) <0.001. g The potency of Sp in maintaining mitochondrial redox balance in paraquat-induced oxidative stress model was tested by exposing Oregon R⁺ Drosophila flies to 10 mM paraquat (PQ), followed by 24 h co-treatment with 2.5 mM Sp. Bars represent fold change of mt-roGFP fluorescence intensity (FI) over untreated flies, as mean ± s.e.m.; n = 10, **P (t-test) <0.001. UT – untreated with Sp.