Silymarin attenuates escitalopram (cipralex) induced pancreatic injury in adult male albino rats: a biochemical, histological, and immunohistochemical approach

Abstract

Depression is a prevalent global problem since ages, predominately treated with SSRI. Cipralex, is an antidepressant of the SSRIs class used as a remedy for mood, depression and anxiety. Silymarin (SIL), a natural free radical scavenging, has an antioxidant and anti-inflammatory properties. This hypothesis evaluates, for the first time, the role of cipralex on the structure of the endocrine and exocrine components of the pancreas and assess the beneficial effects of SIL on these changes. Forty-five rats were divided into control, cipralex, and cipralex plus SIL groups. During sacrifice, all rats and pancreases were weighed and the ratio of pancreatic weight (PW) to rat weight (RW) was calculated, blood samples were collected to estimate fasting glucose, insulin and amylase levels, the specimens were prepared for histological, immunohistochemical (inducible nitric oxide synthase [iNOS], tumour necrosis factor-alpha [TNF-α], caspase 3, proliferating cell nuclear antigen [PCNA], and anti-insulin antibody), and morphometrical studies. Cipralex group exhibited marked destruction of the pancreatic architecture of the exocrine and endocrine parts, with a dense collagen fiber deposition. Also, there is highly significant decrease (P<0.001) of PW/RT ratio, insulin, and amylase levels, the number and diameter of islets of Langerhans, the number of PCNA positive immunoreactive cells, and the number of insulin positive β-cells. Furthermore, a highly significant increase of glucose level, iNOS, TNF-α, and caspase-3 positive immunoreactive cells in the islets of Langerhans and acinar cells were observed. SIL improves the pancreatic histological architecture, weight loss, biochemical, and immunohistochemical analyses. Administering SIL is advantageous in managing cipralex induced pancreatic injury via its anti-inflammatory, antioxidant, and anti-apoptotic qualities.

Gastrodin improves nerve cell injury and behaviors of depressed mice through Caspase‐3‐mediated apoptosis

“…The pathogenesis of depression is complex, which may be related to low psychological and mental activities resulting from the decrease of brain neurotransmitters, 19 as well as to the elevation of inflammatory cytokines caused by hormonal abnormalities. The injury of nerve cells is an important pathological mechanism inducing depression, 20,21 and the apoptosis signaling mediated by Caspase‐3 and Caspase‐9 is one of the major mechanisms of nerve cell death 22 . Expressions of multiple inflammatory factors can promote the activation of Caspase‐3/9 signaling to induce nerve cell damage 23 .…”

“…The injury of nerve cells is an important pathological mechanism inducing depression, 20,21 and the apoptosis signaling mediated by Caspase-3 and Caspase-9 is one of the major mechanisms of nerve cell death. 22 Expressions of multiple inflammatory factors can promote the activation of Caspase-3/9 signaling to induce nerve cell damage. 23 GAS has been proven to possess potent antioxidant and antiinflammatory effects, which has also been reported to have the depression-ameliorating function.…”