The current study investigated the protective potential of Azolla pinnate ethanolic extract (APE) against lead-induced hepatotoxicity in rats. Sixty male Wistar albino rats were randomly allocated into six groups (n = 10). The control group was orally administrated with saline. The second group received lead acetate (100 mg/kg body weight (BW) orally for 60 days). The third group was fed with APE (10 mg/kg BW orally for 60 days). The fourth group was administrated with lead acetate like the second group and APE like the third group, concomitantly, for 60 days. The fifth group was administrated with APE like the third group for 30 days, then orally administrated with the lead acetate like the second group for another 30 days. The sixth group was administrated with lead acetate like the second group for 30 days, then with APE like the third group for a further 30 days. Phytochemical analysis of APE indicated the presence of peonidin 3-O-glucoside cation, vitexin, rutin, thiamine, choline, tamarixetin, hyperoside, astragalin, and quercetin. The latter has been elucidated using one- and two-dimensional nuclear magnetic resonance (1D and 2D NMR) and liquid chromatography–mass spectrometry (LC–MS-MS). Lead acetate increased the serum levels of alanine and aspartate aminotransferases and that of urea, creatinine, tumor necrosis factor alpha, and interleukin 1β, hepatic tissue malondialdehyde contents, and caspase 3 protein expression, as well as altering the hepatic tissue architecture. However, it decreased the serum levels of interleukin 10 and glutathione (GSH) contents, and the activities of catalase and superoxide dismutase in hepatic tissue. In contrast, the administration of APE ameliorated the lead-induced alterations in liver function and structure, exemplifying the benefits of Azolla’s phytochemical contents. Collectively, A. pinnate extract is a protective and curative agent against lead-induced hepatotoxicity via its antioxidant, anti-inflammatory, and anti-apoptotic impacts.

This study was performed to evaluate anti-obesity potential of Commiphora myrrha resin ethanolic extract (CME) with the respect to expression of leptin, adiponectin and uncoupling protein 1 (UCP1) in rats. Control rats fed basal diet. Second group fed basal diet and administered CME (500 mg/kg bw) orally for 14 weeks. Third group fed high fat diet (HFD) for 14 weeks. Fourth group fed HFD and administered CME as second group. Fifth group fed HFD for 8 weeks then fed basal diet and administered CME as third group for another 6 weeks. Phytochemical analysis of CME identified the presence of germacrene B, 1,4-benzoquinone, benzofuran, hexadecanoic acid, 9,12-octadecnoic acid methyl ester, reynosin, 11, 14-eicosadienoic acid, isochiapin B, bisabolene epixod, elemene and 1-heptatriacotanol. High fat diet significantly increased food intake, body weight, hyperglycemia, serum levels of total cholesterol, triacylglycerol, low density lipoprotein and ketone bodies, AST and AST activities, concentration of malondialdehyde and histopathological changes in hepatic tissues. However, it significantly reduced serum levels of high density lipoprotein, leptin and adiponectin, activity of hepatic glutathione reductase (GR) and brown adipose tissue UCP1 protein expression. In contrast, CME ameliorated HFD increased body weight, hyperglycemia, dyslipidemia, ketonemia, hepatic tissues lipid peroxidation, restored hepatic tissue architecture and enhanced protein expression of leptin, adiponectin and UCP1 and activity of hepatic GR. This study indicated that CME ameliorated HFD induced hyperglycemia and dyslipidemia through normalization of HFD reduced leptin, adiponectin and UCP1 proteins production and antioxidant activity.

This study examined the protective effect of earthworm extract (EE) on acrylamide (ACR)-induced reproductive dysfunction. Forty male rats were allocated into four groups (n = 10). The G I (control) group received distilled water (D.W.). The G II group received ACR (5 mg kg⁻¹ B.W. in D.W.) 5 days per week, orally, for 3 weeks. The G III group was administered EE (300 mg kg⁻¹ B.W in D.W.) 5 days per week, orally, for 3 weeks. The G IV group was pretreated with EE for 3 weeks and then co-treated with EE and ACR for an additional 3 weeks. ACR decreased the number of sperm, sperm viability, and total motility. However, it increased testosterone levels with no effect on the FSH or LH levels. Moreover, ACR increased the concentrations of malondialdehyde (MDA) and nitric oxide (NO). Meanwhile, it decreased the glutathione (GSH) concentration in testicular tissues. Notably, the expression levels of p53 and Ki-67 were increased in the degenerated spermatogenic cells and in the hyperplastic Leydig cells of the testis of the ACR-treated group, respectively. Acrylamide induced alterations in the testicular tissue architecture. Interestingly, EE restored the sperm parameters and recovered the testicular histological structures and the biochemical alterations induced by ACR. In conclusion, earthworm extract ameliorated ACR-induced reproductive toxicity via restoring the testicular antioxidant balance and suppressing p53 and Ki-67 expressions in testicular tissues.