**Figure 6.**

*Biological properties and chemical constituent of Red Chili.*

Capsaicin treatment ameliorated lipid peroxidation, inhibited myeloperoxidase activity in gastric lesions (ethanol induced) in rats [120].

Dried red chili powder (1% w/v) showed inhibitory effects against *Listeria monocytogenes* [121]. Tropical application of capsaicin (0.075%) reduced fat accumulation in mesenteric and epididymal adipose tissue by increasing expression of adipokines [122]. It was also found that a dose of 200 mg/kg of capsaicin decreases plasma triglyceride levels and fasting glucose in obese mouse model kept on high fat diet [123].

Earlier studies suggested the risk of oral cavity [124] and stomach [125] cancer on consumption of red chili, however, recent reports suggested that consumption of red chili is safe and does not increase risks of cancer [126]. Numerous reports have suggested protective effects of capsaicin against cancer. Capsaicin showed inhibitory effects on the growth of human KB cancer cells by promoting apoptosis at a concentration of 200–250 μM [127]. Further, capsaicin led to the formation of reactive oxidative species through mitochondria (at a dose of 150 μM) causing loss in mitochondrial membrane potential in BxPC-3 and AsPC-1, human pancreatic cancer cell lines [128]; inhibited activation of NF-kB and AP-1, transcription factors responsible for cellular proliferation and malignant formation, in mice model [129]. In addition, capsaicin inhibited growth of MCF breast cancer cell lines by causing cell cycle arrest at S phase and induced poly(ADP-ribose) polymerase-1 (PARP-1) cleavage (apoptosis is marked by the cleavage of PARP-1) by activating caspase-7 which is involved in apoptosis (**Figure 6**) [130]. Capsaicin and cisplatin, in a synergistic manner, arrested the growth of SNU-668, human gastric cell line at G1/S phase [131].
