Fig. 7: Harmol activates the AMPK-mTOR-TFEB pathway and enhances autophagy and lysosome biogenesis in A53T α-syn mice. | npj Parkinson's Disease

Fig. 7: Harmol activates the AMPK-mTOR-TFEB pathway and enhances autophagy and lysosome biogenesis in A53T α-syn mice.

From: Harmol promotes α-synuclein degradation and improves motor impairment in Parkinson’s models via regulating autophagy-lysosome pathway

Fig. 7: Harmol activates the AMPK-mTOR-TFEB pathway and enhances autophagy and lysosome biogenesis in A53T α-syn mice.

a A53T α-syn mice were treated with 10, 20, and 40 mg/kg harmol for 1 month. Substantia nigra were homogenized and extracted for Western blot analysis. Representative blots of p-AMPK, AMPK, p-mTOR, mTOR, and TFEB are shown. b The levels of p-AMPK/AMPK, and p-mTOR/mTOR, and TFEB were quantified as the mean ± SEM. #P < 0.05, ##P < 0.01 and ###P < 0.001 vs. the wild-type (saline). *P < 0.05 and ***P < 0.001 vs. the A53T Tg. c A53T α-syn mice were administered with 10, 20, and 40 mg/kg harmol for 1 month. The levels of the LC3B-II/LC3B-I, pro-CTSD, mature-CTSD, p-ULK1 (Ser757), p-ULK1 (Ser317), p-ULK1 (Ser555) and ULK1 in substantia nigra were determined by western blot. Representative blots are shown. The expression of p-ULK1 (Ser757)/ULK1 (d), p-ULK1 (Ser317)/ULK1 (e), p-ULK1 (Ser555)/ULK1 (f), pro-CTSD (g), mature-CTSD (h), and LC3B-II/LC3B-I (i) was quantified as the mean ± SEM. #P < 0.05, ##P < 0.01 and ###P < 0.001 vs. the wild-type (saline). *P < 0.05, **P < 0.01 and ***P < 0.001 vs. the A53T Tg.

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