Table 2.

Biologically active compounds targeting cell death pathways in H. pylori infection.

Programmed cell death	Compound	Mechanism of action	References
Apoptosis	Tanshinone IIA Quercetin L-ascorbic Acid-2-Glucoside Eudesmin Lactobacillus rhamnosus JB3	Increases apoptotic relevant protein BAX and caspase-9 expressions in H. pylori infection. Affects the levels of BCL-2 and BAX to protect against apoptosis associated with H. pylori infection. Improves mitochondrial function by restoring the level of ATP and MMP, inhibits H. pylori induced apoptosis. Suppresses the activation of apoptosis associated proteins induced by H. pylori. Inhibits intrinsic apoptosis proteins including BAX, cytochrome c, and caspase-3 mediated by infection.	(Chen et al., 2016) (Zhang et al., 2017c) (Chen et al., 2018) (Yang et al., 2018) (Do et al., 2021)
Autophagy	Chloroquine Glycyrrhizin Simvastatin Astaxanthin	Inhibits the increased expression of Beclin1 and LC3B-II, thereby reducing autophagy in H. pylori infection. Restores autolysosomal function by inhibiting HMGB1 to ameliorate H. pylori infection. Enhances early endosome maturation and subsequently activates the autophagy pathway. Induces autophagy through the activation of AMPK and the downregulation of its downstream target, mTOR.	(Li et al., 2023) (Khan et al., 2023) (Liao et al., 2016) (Lee et al., 2020)
Pyroptosis	Rabeprazole	Inhibits pyroptosis by alleviating GSDMD-executed pyroptosis, leading to decrease IL-1β and IL-18 mature and secretion.	(Xie et al., 2021)

ATP, Adenosine triphosphate; MMP, Mitochondrial membrane potential; HMGB1, High mobility group box 1; AMPK, Adenosine monophosphate-activated protein kinase; mTOR, Mammalian target of rapamycin.